Chapter 85 – Physiology of Ageing

Abstract

Ageing involves processes not only of physical but also of psychological and social change. Increasing numbers of elderly people are undergoing elective and emergency surgery, with post-operative complications being more common in the older population. It is important to understand the normal changes that occur with advancing age so that anaesthetic techniques can be modified and to allow early identification of anaesthetic and surgical complications.

Chapter 85 Physiology of Ageing

What makes surgery and anaesthesia in older people higher risk?

Whilst the chronological age of a patient is easily measured (i.e. years), a patient’s functional age is both more important and more difficult to measure. Ageing is associated with a decline in the physiological reserve of every organ system. The mechanism of this decline is either loss of cells from an organ or reduced function of the remaining cells. The decline in organ function often begins early in adult life, but is often not clinically evident until almost all of the organ reserve is lost. Organ failure occurs either when organ function declines to a level that can no longer support life or when a disease state requires an increase in organ function that cannot be met due to insufficient reserve.

Older patients often have chronic diseases that may impact the development or progression of an acute illness. The polypharmacy that commonly accompanies chronic illness may also influence the medical and anaesthetic management of an acute illness.

Describe the physiological and anatomical changes of interest to anaesthetists

The physiological and anatomical changes associated with ageing can be classified according to organ system:

Respiratory system:
1. – Airway. The elderly are often edentulous, making bag–valve–mask ventilation more difficult, but intubation easier.
2. – Upper airway collapse. The upper airway becomes more prone to collapse, particularly at night: partial obstruction (snoring) and arterial hypoxaemia are common. Decreased upper airway tone can be problematic during recovery from anaesthesia, with airway obstruction being more common.
3. – The thoracic cage. With advancing age:
  1. ▪ The thoracic cage becomes more rigid due to calcification of the coastal cartilages, leading to reduced thoracic wall compliance.
  2. ▪ Vertebral column deformity leads to kyphosis, which adversely affects lung mechanics.
  3. ▪ The diaphragm and intercostal muscles atrophy. At times of high respiratory workload, this makes the elderly more susceptible to respiratory muscle fatigue.
4. – Degeneration of the elastic fibres of the alveolar septae, leading to:
  1. ▪ Loss of support for alveoli and small airways, resulting in airway collapse in expiration (i.e. an increased closing capacity, CC). This is a major cause of V̇/Q̇ mismatch and hypoxaemia in the elderly (see Chapter 15).
  2. ▪ Increased lung compliance, which partially offsets the reduced thoracic wall compliance. Overall, the combined respiratory compliance is lower in older patients; that is, the gradient of the pressure–volume curve is reduced (Figure 85.1).
  3. ▪ An increase in residual volume and functional residual capacity (FRC) (Figure 85.2). FRC occurs at the point where the inward elastic forces match the outward spring of the thoracic cage. Reduced lung elastic recoil means that FRC occurs at increased lung volume. The anterior–posterior diameter of the lung increases as a consequence of the higher resting lung volume. This results in flattening of the hemi-diaphragms, putting them at a mechanical disadvantage; the energy expended during inspiration increases.
5. – Alveolar–arterial (A–a) O₂ gradient increases with age. This is in part due to V̇/Q̇ mismatch associated with increased CC, but is also due to:
  1. ▪ Reduced diffusing capacity of the alveoli due to both reduced alveolar surface area and increased alveolar–capillary membrane thickness;
  2. ▪ Hypoxic pulmonary vasoconstriction being less active, which further exacerbates V̇/Q̇ mismatch.
Cardiovascular system:
1. – Arteries stiffen with age, leading to systolic hypertension. This has two effects:
  1. ▪ The walls of the aorta normally distend to accommodate the blood ejected from the left ventricle (LV). With ageing, the LV must generate a greater pressure to eject the stroke volume into a stiff aorta.
  2. ▪ Normally, ejection of blood into the aorta causes a pressure wave that passes along the aorta and is reflected back towards the heart. The reflected wave reaches the heart after ejection of blood is complete and is responsible for the bump after the dicrotic notch in the arterial waveform. In the elderly, stiffened arteries cause an increase in the speed of the pressure wave. The reflected wave consequently reaches the heart in late systole, which further increases the pressure against which the ventricle must pump.
1. – Left ventricular hypertrophy. As a consequence of the increase in afterload, the LV undergoes hypertrophy. Ventricular hypertrophy increases the stiffness of the LV, which impairs diastolic relaxation (see Chapter 30). This diastolic dysfunction worsens with age. The heart becomes progressively more dependent on atrial contraction for ventricular filling. This is why development of atrial fibrillation (AF) can so easily result in LV failure in the elderly.
2. – Veins stiffen with age. Normally, veins act as a reservoir of blood to buffer changes in venous pressure, maintaining a constant right ventricular preload. With increasing age the veins stiffen, reducing their compliance and impairing the buffering mechanism. This is why the elderly are more likely to become hypotensive with mild hypovolaemia.
3. – Decreased response to β-adrenergic stimulation with ageing, causing:
  1. ▪ Reduced responsiveness of heart rate (HR) to catecholamines during exercise, resulting in a reduced maximum HR. Resting HR is unchanged.
  2. ▪ The baroreceptors are less able to rapidly reflexively modify HR in response to changes in blood pressure, predisposing the elderly to postural hypotension.
4. – Cardiac output (CO) falls with age at a rate of approximately 1% per year. This is due to reduced contractility of the LV as a result of both the reduced response to β-adrenergic stimuli and reduced myocyte function with advancing age.
5. – Conduction system abnormalities. There is an increased tendency to supraventricular arrhythmias, particularly atrial and ventricular ectopic beats, and AF. This is thought to be due to fibrosis of the atria and sinoatrial node, as well as a large reduction in the number of pacemaker cells.
6. – Cardiac valve degeneration. Calcification of the aortic valve is more common in older patients, leading to aortic sclerosis and aortic stenosis.
Central nervous system:
1. – Loss of brain cells. A generalised loss of cells leads to a reduced brain weight and the appearance of cerebral atrophy on computed tomography scan. The remaining neurons compensate by forming longer dendrites and making more connections to other neurons. Loss of dopaminergic neurons results in Parkinson’s disease, whilst loss of cholinergic neurons in the hypothalamus is implicated in the development of dementia. The reduction in cell number results in a lower cerebral metabolic O₂ demand; cerebral blood flow is reduced by 10–20% as a result of the lower metabolic demand.
2. – Sensory impairment is common. Deafness is very common in older people, and visual impairment affects around a third of the elderly population.
3. – Cognitive impairment becomes more common with advancing age, affecting 20% of patients aged over 80.
Renal physiology:
1. – Decrease in glomerular filtration rate. Young adults have a significant reserve in renal function. From the age of 30 years, there is a progressive loss of glomeruli and reduced renal plasma flow, resulting in a lower creatinine clearance.
2. – Obstructive nephropathy is common in elderly men due to prostatism.
Hepatic physiology:
1. – Reduced liver size and hepatic blood flow with advancing age. This results in reduced hepatic drug clearance.
2. – Decreased synthesis of plasma proteins with advancing age. Of note, albumin concentration decreases and plasma cholinesterase levels are reduced.
Endocrine system: diabetes mellitus is common in the elderly. There is an increase in peripheral insulin resistance and impaired insulin secretion in response to hyperglycaemia.
Locomotor and skin:
1. – The elderly tend to have reduced subcutaneous tissue, thin skin and fragile veins; achieving venous access can be difficult. Infusions of fluids or drugs can extravasate, especially if introduced under pressure. Pressure sores are more common, and additional care must be taken with patient positioning and padding of pressure points.
2. – There is a generalised loss of muscle mass with advancing age, known as sarcopenia; 6 kg of muscle is lost by 80 years of age. This is thought to be due to loss of motor neurons, resulting in decreased levels of Ca²⁺ within the sarcoplasm.
3. – Arthritis and bony deformities are very common in older people. This may lead to difficulty with mobility and positioning, potentially making regional anaesthesia more difficult. Larger-calibre spinal needles may be required to pass through calcified ligaments. Fortunately, post-dural puncture headache is far less common in the elderly.
Thermoregulation is impaired with advancing age:
1. – The elderly are at risk of hypothermia due to a reduction in heat production: basal metabolic rate decreases by 1% per year, and there is a reduction in the peripheral vasoconstrictor response to cold exposure.
2. – Older patients are especially at risk of intraoperative hypothermia. Post-operative shivering is the normal mechanism of returning to normothermia. The elderly may lack the muscle bulk to shiver effectively or may have insufficient cardiopulmonary reserve to meet the increased O₂ demand of shivering. Prevention of perioperative hypothermia in the elderly is crucial.
3. – The elderly are also at risk of hyperthermia due to impairment of sweating.
Body compartments:
1. – A reduced blood volume and a higher proportion of body fat can lead to changes in the volume of distribution.
2. – Plasma protein concentration is reduced, resulting in decreased drug protein binding, an increase in the free drug fraction and thus a higher free drug concentration.