LITMIR.BIZ

Скачать книгу

deaths were from CAD (predominantly as a result of MI) and this equates to around 74,000 deaths (British Heart Foundation, 2014). CAD is usually diagnosed using a stress ECG (S-T depression) and subsequent angiography which allows the diameter of the coronary arteries to be visualised.

      CAD and angina pectoris

      As coronary vessel occlusion progresses in CAD patients, less oxygenated blood is delivered to the myocardium and the cardiac muscle cells are forced into anaerobic respiration with lactic acid accumulation. This build-up of lactic acid produces a heavy sensation that is often experienced as central chest pain behind the breastbone. This painful sensation that is associated with CAD is referred to as angina pectoris and commonly spreads from the chest, down the left arm and frequently up the left side of the neck into the left side of the jaw.

      Angina can be subdivided into stable angina, where the pain is brought on following physical exertion such as walking up a hill, and unstable angina, where the pain is often unpredictable, frequently occurring without physical exertion at apparently random times during the day and night. Unstable angina is a serious clinical finding since it is often seen in patients prior to suffering an MI.

      CAD and myocardial infarction (MI)

      A major danger with progressive CAD is that narrowed coronary arteries can easily become completely blocked by a thrombus (clot) or a dislodged piece of fatty plaque. Frequently an area of plaque will rupture, activating the clotting cascade, leading to rapid thrombosis and total vessel occlusion that is indicative of an MI (heart attack).

      During infarction the cardiac muscle cells of the myocardium are deprived of oxygen and begin to die. Most MIs result in a characteristic, concentric pattern of tissue damage made up of the area of necrosis (dead tissue), the area of injury (living but damaged tissue) and the ischaemic zone (healthy living tissue but with reduced oxygen supply).

      All three concentric areas surrounding the occlusion will collectively reduce the heart’s ability to function as an effective pump.

      Although MI can come on suddenly and without warning, often a variety of symptoms are initially present. These can include chest pain, shortness of breath (dyspnoea), increased sweating (hyperhidrosis), feeling of impending doom (severe anxiety), confusion or lethargy (NHS, 2018); you may remember all of these were present in George’s case study at the beginning of this chapter. However, not everyone will experience MI in the same way; older women often present atypically with research indicating that less than half of women over the age of 75 experienced chest pain during MI (Milner et al., 2004).

      To develop your knowledge of heart disease, read through Gloria’s case study before attempting Activity 3.3.

      Case study: Gloria – peripheral oedema

      Gloria is a chatty 86-year-old woman living on her own in sheltered accommodation. For the last 20 years she has suffered chest pain on exertion and five years ago she suffered a major MI followed by two less serious infarctions. Gloria has had stents fitted but based on her health was judged as not fit enough for bypass surgery. During your visit Gloria has been complaining of swollen feet and ankles which, while not painful, are preventing her from wearing even her slippers.

      Nurses are required to carefully assess the health status of their patients and draw accurate conclusions based on medical history and current observation.

      Activity 3.3 Critical thinking

      Based solely on the information that has been provided in the case study, what conclusions can you draw about Gloria’s clinical history and the possible cause of her ankle and foot swelling?

      We have now examined the structure and function of the heart and blood vessels which work together to enable adequate circulation for healthy tissue perfusion. To ensure that blood is delivered to all regions of the body, an adequate blood pressure must be maintained and regulated.

      Blood pressure

      Nurses routinely measure blood pressure (BP) using a device termed a sphygmomanometer (sphyg). Because of the past history of using mercury column sphygs (rarely used today because of the toxicity of mercury), BP readings recorded using digital, mercury-free devices are still expressed in mmHg.

      A typical reading in a young, healthy adult would be around 120/80 mmHg.

      The two figures obtained each time a blood pressure measurement is taken represent:

       The systolic BP: This is the upper figure which corresponds to the time during the cardiac cycle when the ventricles are undergoing systole (contraction) and blood is being ejected.

       The diastolic BP: This is the lower figure and corresponds to the time during the cardiac cycle when the ventricles of the heart are undergoing diastole (relaxation) and no blood is being ejected.

      Currently NICE (National Institute for Health and Care Excellence) recognises BP readings of 140/90 mmHg or higher as being indicative of hypertension (high blood pressure). It is estimated that hypertension affects at least a quarter of all adults in the UK and over half of all adults in the UK over the age of 60. Hypertension is a major preventable cause of mortality in the UK, increasing the risk of MI, stroke (CVA), heart failure, chronic kidney disease and cognitive decline (NICE, 2018).

      A normal BP is essential to maintain tissue perfusion (blood supply) throughout the body from the top of the scalp to the tips of the toes. BP can be affected by many parameters, but a normal BP depends on having a healthy heart to ensure adequate cardiac output (CO) and healthy blood vessels to ensure adequate blood flow. The blood vessels provide a collective resistance to blood flow with the total resistance offered by all the blood vessels in the body known as the peripheral resistance (PR).

      In simple terms BP can be thought of as a product of multiplying the CO and the PR:

      BP = CO × PR

      As we will explore below, BP can be altered by changing the heart rate to change CO or by altering the diameter of blood vessels to change the PR.

      Control of BP

      The human body has a variety of elaborate homeostatic mechanisms to ensure that BP is maintained within its normal range. BP control can be broadly split into neural mechanisms, which allow BP to be altered rapidly within seconds, and hormonal mechanisms, which play a key role in the medium- to long-term control of BP.

      Neural control of BP

      Two specialised regions are located within the medulla oblongata (inferior portion of the brain stem) which can rapidly either raise or lower the BP to match the body’s current needs. The cardioregulatory centre or cardiac centre regulates the heart rate and hence the cardiac output (CO). The vasomotor centre regulates vascular tone by controlling the diameter of blood vessels (vasodilation or vasoconstriction). By regulating vascular tone, the vasomotor centre is able to increase or decrease the peripheral resistance (PR).

      Both the cardiac and vasomotor centres require a continuous ‘real-time’ measurement of the current BP. This is achieved using specialised stretch receptors called baroreceptors which are located in the walls of the aortic arch and carotid sinuses (bulbous regions of the carotid arteries in the neck). Measuring the degree of stretch gives a good measure of current BP, with more stretch equating to a higher BP and less stretch indicative of a lower BP. In humans the aortic arch baroreceptors relay information to the cardioregulatory and vasomotor centres via the vagus nerve and the carotid sinus baroreceptors via the glossopharyngeal nerve (Figure 3.10).

      Figure 3.10 Baroreceptor response

      The baroreceptor responses

      Neural

Скачать книгу