Chapter 14: Observations
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Source: Marini and Dries ([112]).
Related theory
Blood pressure is determined by cardiac output and vascular resistance and can be described as shown in the equation in Box 14.2. If that equation is combined with the equation for cardiac output (see Box 14.1), which uses heart rate (HR) and stroke volume (SV), blood pressure (BP) could be seen as (Blows [21]):
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In theory, anything that alters one of the above components (stroke volume, heart rate or systemic vascular resistance) will therefore produce a change in blood pressure (Tortora and Derrickson [199]). However, this is not always the case as a drop in one may be compensated for by an increase in either of the others (Patton [155]).
Box 14.2
Blood pressure equation
| BP | = | CO | × | SVR |
| (blood pressure) | (cardiac output) | (systemic vascular resistance) |
Normal blood pressure
Normal blood pressure ranges between 100 and 140 mmHg systolic and 60 and 90 mmHg diastolic at rest (Lough [105]). However, it varies depending on age (increasing with age), activity, sleep, emotion, positioning, physical condition and fitness (Tortora and Derrickson [199]). It also varies depending on the time of day, being at its lowest during sleep (Blows [21]). Blood pressure therefore reflects individual variations but an abnormal blood pressure should not be assumed to be the individual's norm; rather, it should be assessed in relation to their previous results, general condition and other observations (Bunce and Ray [33]).
Hypotension
Hypotension is generally defined in adults as a systolic blood pressure below 100 mmHg (Marieb and Hoehn [110]). A low blood pressure may indicate orthostatic hypotension – that is, a sudden drop in blood pressure when the patient rises from a supine or sitting position (Brown and Cadogan [31]). This is usually compensated for by the baroreceptor reflex and the sympathetic nervous system but, especially in older people, this compensatory mechanism may not work as efficiently (Marieb and Hoehn [110]). Hypotension can also be a symptom of many other conditions, including shock, haemorrhage and malnutrition, all of which can result in reduced tissue perfusion and lead to hypoxia and an accumulation of waste products (Sprigings and Chambers [189]).
Hypertension
Hypertension is defined as blood pressure of 140/90 mmHg or greater and can be either primary hypertension, with no single known cause, or secondary hypertension, which means it is related to another factor such as kidney disease (NICE [132]).
Factors leading to hypertension include sex, genetic factors and age, alongside risk factors such as obesity, lack of exercise, smoking, and high caffeine and/or alcohol intake (Patton [155]). If hypertension is sustained, the heart will have an increased workload to maintain circulation; greater stress will be placed on the blood vessel walls and cardiac ischaemia can occur (Wilkinson et al. [215]).
There are many illnesses and factors that can lead to changes in blood pressure (Figure 14.20), and hypertension is one of the most important preventable causes of premature morbidity and mortality in the UK (NICE [132]). It has been suggested that a patient's knowledge of their own ‘goal blood pressure’ is associated with improved blood pressure control (NICE [132]). Interventions to improve knowledge of specific blood pressure targets may have an important role in optimizing blood pressure management (NICE [132]).
Figure 14.20 Factors that lead to an increase in blood pressure. Changes noted within green boxes increase cardiac output, whereas changes noted within blue boxes increase systemic vascular resistance. Source: Reproduced from Tortora and Derrickson ([199]) with permission of John Wiley & Sons.
Mean arterial pressure
The mean arterial pressure (MAP) is the average pressure of blood throughout the pulse cycle and thus is a reliable indication of perfusion (Lin [104]). Mathematically, the MAP is derived from the diastolic pressure and the pulse pressure (which is the difference between the systolic and diastolic blood pressures) (Marieb and Hoehn [109]):
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Therefore, a patient with a blood pressure of 123/90 mmHg has a MAP of 101 mmHg. An adequate MAP is usually deemed to be between 65 and 70 mmHg (Marini and Dries [112]).
Resistance
Resistance is effectively the opposition to blood flow and is created by friction between the walls of blood vessels and the blood itself (Patton [155]). It is termed ‘peripheral’ or ‘systemic’ vascular resistance because most of the resistance occurs in the vessels away from the heart (Marieb and Hoehn [110]). Systemic vascular resistance varies depending on the degree of vasoconstriction or vasodilation, the viscosity of blood and the length of the vessels, although the last two factors generally remain relatively static (Marieb and Hoehn [110]). Arterioles can dilate or constrict; when they are constricted, systemic vascular resistance increases and blood flow to the tissues decreases, increasing the arterial blood pressure (Patton [155]). The blood pressures in the vessels of the cardiovascular system can be seen in Figure 14.21.
Figure 14.21 Blood pressures in various parts of the cardiovascular system. The white line is the mean (average) blood pressure in the aorta, arteries and arterioles. Source: Reproduced from Peate and Wild ([157]) with permission of John Wiley & Sons.
Blood pressure control
Hormonal control
Many hormones help to regulate blood pressure, including adrenaline and noradrenaline, which are released from the adrenal medulla in response to a drop in blood pressure; these hormones increase cardiac contractility and vasoconstriction, and thus increase cardiac output (Patton [155]). Atrial natriuretic peptide is a hormone that is produced from the atria of the heart in response to hypertension. It works by inhibiting the renin–angiotensin system, raising the glomerular filtration rate by causing vasodilation in the afferent arteriole, inhibiting sodium reabsorption and causing fluid transfer into the interstitial space (Waugh and Grant [207]) in an attempt to lower blood pressure.
Neural control
When blood pressure increases, the baroreceptors, or stretch receptors, are stimulated and in turn stimulate the cardiac inhibitory centre, reducing sympathetic nerve impulses and increasing parasympathetic nerve impulses (Marieb and Keller [111]). This causes vasodilation and a decrease in cardiac output, thereby reducing blood pressure (Blows [21]). When blood pressure is low, the opposite occurs. This response is termed a ‘reflex arc’, and it continually maintains homeostasis (Marieb and Hoehn [110]). Baroreceptors are located in the aortic arch, the carotid sinuses and the walls of most of the large arteries in the thorax and neck (Marieb and Hoehn [110]). Close to these are chemoreceptors, which are stimulated when the pH of the blood drops or when carbon dioxide rises, and when oxygen levels drop significantly; this causes an increase in cardiac output and vasoconstriction, leading to an increase in blood pressure (Marieb and Hoehn [110]).
Renal control
The juxtaglomerular cells within the kidneys are stimulated to release renin when blood volume or pressure falls (Tortora and Derrickson [199]). This leads to the production of angiotensin I, which is converted to angiotensin II (with the aid of angiotensin‐converting enzyme) (Patton [155]). Angiotensin II has a potent effect on blood pressure, increasing cardiac output and vasoconstriction and stimulating the production of aldosterone. Aldosterone increases reabsorption of water and sodium and stimulates the thirst receptors (Patton [155]) in an attempt to increase the circulatory volume of fluid and thereby blood pressure (Blows [21]). These mechanisms are known collectively as the renin–angiotensin–aldosterone system (Figure 14.22). Anti‐diuretic hormone is produced in the hypothalamus in response to low blood pressure or volume and increases vasoconstriction and water reabsorption in the kidneys. These mechanisms are inhibited when fluid volume in the circulatory system is high (Marieb and Keller [111]).
Figure 14.22 The renin–angiotensin–aldosterone system. Source: Reproduced with permission of Soupvector – Own work, CC BY‐SA 4.0 https://commons.wikimedia.org/w/index.php?curid=66583851.
Other mechanisms that influence blood pressure
Skeletal muscle contractions and the mechanism of respiration promote venous return of blood to the heart and therefore assist in maintaining cardiac output (Lin [104]). Skeletal muscles contract on movement, compressing the veins and pushing the blood towards the heart, and respiration causes a change in thoracic and abdominal pressure, which acts to pump venous blood (Patton [155]). Starling's law states that the force of the contraction of the heart is directly related to how much blood volume is in the heart (Patton [155]). The more stretched the muscle fibres are prior to contraction, the stronger the contraction and the greater volume the heart will pump (Marieb and Keller [111]).
