This chapter is relevant to the grim warning at the front of the 2017 CICM Primary Syllabus, which threatens the exam candidate that "for all sections of the Syllabus an understanding of ... physiology at the extremes of age... is expected". If so, then it is not expected with the same ardour as many other subjects, as it has only ever appeared once in the exam. Question 19 from the first paper of 2015 asked the candidates to "describe the effects of ageing on the cardiovascular system", generating a pass rate of 29%. For the remaining 71%, this chapter offers a short summary of the main points.
- Structural changes:
- LV hypertrophy
- Interventricular septal hypetrophy
- LVOT narrowing
- Valvular sclerosis
- Degeneration of sympethetic innervation
- Dilation of aorta and large arteries
- Thickening of arterial walls
- Decreased windkessel effect
- Functional changes:
- Increased systolic function
- Decreased diastolic function
- Increased atrial diastolic contribution (atrial "kick")
- Decreased cardiac output (by 1% per year)
- Decreased maximal heart rate
- Increased cardiac workload (due to afterload increase)
- Blunted baroreceptor reflexes
- SA node atrophy
- Conductive tissue loss
- Action potential prolongation
- Decreased arterial compliance
- Decreased endothelial NO-mediated vasodilatory function
- Systolic blood pressure increases
- Pulse pressure increases (diastolic pressure increases less than systolic)
- Pulmonary arterial pressure increases
- Increased ANP secretion
- Increased circulating catecholamine levels
- Decreased renin, angiotensin and aldosterone concentrations
Normal age-related changes are the subject here. Sure, your coronary arteries might be overgrown with greasy calcified stalactites and your mitral annulus might have dilated hideously, but those are pathological changes, old man - they have nothing to do with the beautiful natural process of ageing. The best account of this noble dignified descent into the wormy grave is offered by Karavidas et al (2010), which also happens to be free. Unless otherwise stated, everything in the summary below comes from this article. Alternatives include Safar (1990), Ribera-Casasado (1999) and Ferrari et al (2003). These aren't free, and given the relative neglect of this topic in the CICM exams, there's probably no point wasting your time reviewing them, as the authors themselves will remind you that life is short.
Effects of ageing on myocardial structure
- Ventricular hypertrophy: the left ventricular wall increases in thickness, and this is apparently something that happens even in the absence of chronic hypertension. Hypertrophy here occurs for individual myocytes: overall the number of the cells is reduced by 30-35% between the age of 17 and the age of 90, but the remaining cells are larger, leading to an overall increase in ventricular wall thickness.
- Changes in cardiac morphology: "An age-dependent change in cardiac shape has been described, with a rightward shift in the ascending aorta and a proximal bulge in the interventricular septum, which entail a narrowing of the left ventricular outflow tract", report Ferrari et al (2003).
- Cardiac sympathetic innervation degenerates. McLean et al (1983) were able to demonstrate this in animals ("sympathetic axonal degeneration", they said).
- Aortic sclerosis and incompetence: stiffening, scarring and calcification of the aortic valve leaflets occurs as a lifelong process, and 80% of older people end up with a sclerotic aortic valve. It is sufficiently common to pass for "normal". According to Safar (1990), "mucoid degeneration of collagen in atrioventricular valves" is responsible.
Effects of ageing on myocardial function
- Increased systolic function: Ageing is generally associated with an increase in systolic isovolumic contraction velocity, at least among men (in women it stays the same). This is the rate of contaction during the isovolumic part of the cardiac cycle, measured by echo (Ruan and Nagueh, 2005). Stroke volume and ejection fraction remain stable, according to Ferrari et al (2003).
- Diastolic dysfunction is a normal age-related change, as a result of this decreased ventricular compliance. A Grade I diastolic dysfunction is viewed as normal for all patients over 60. It manifests as impaired LV relaxation and appears as reduced E wave velocity on echo (resulting in E/A ratio reversal to below 1.0).
- Increased late diastolic atrial contribution to LV volume: The atrial "kick" becomes more important with age, particularly as the LV becomes less compliant. Arora et al (1987) conjecture that this is due to atrial remodelling in response to increased atrial afterload.
- Decreased cardiac output: Brandfonbrener et al (1955) determined that cardiac output decreases at a rate of approximately 1% per year. It appears to be maximal in one's twenties, and then it's all downhill from there. This has been confirmed by multiple subsequent studies.
- Decreased maximal heart rate: this also appears to be the consequence of decreased β-adrenergic responsiveness (Christou et al, 2008).
- Increased cardiac workload: even though the cardiac output decreases, because of the increased afterload the total myocardial workload and oxygen consumption.
- Blunted baroreceptor responses: Though resting heart rate remains the same in people of all ages, the variability of heart rate which is normally expected from changes in posture or other baroreceptor stimuli is depressed in old age. Put simply, an old heart does not race as much when stimulated by the autonomic nervous system. This has implications for the haemodynamic responses to haemorrhage and sepsis.
- An overall decreased capacity to meet increased demand: With the baroreceptors malfunctioning, cardiac output decreasing and the vascular endothelium not doing its job, the cardiovascular system is overall less capable of increasing its workload when stress is placed upon it (eg. where exercise or sickness produce and increased demand for cardiac output)
Electrophysiological changes associated with age:
- SA node atrophy: by the time you are 70, of the sinoatrial node cells you were born with, only 10% will remain. Apoptosis is blamed. Similar processes take place all around the myocardium, including in the bundle branches and in the Bundle of His.
- Action potential prolongation: the whole action potential is prolonged, apparently because the L-type calcium channels deactivate more reluctantly. More calcium remains in the cell for longer, which probably influences relaxation and contributes to the diastolic dysfunction.
Effects of ageing on the neurohormonal control systems
- Increased atrial natriuretic peptide but end-organ sensitivity to it is decreased (Ribera-Casasado, 1999).
- Increased circulating catecholamines: authors blame it on the decreased catecholamine receptor sensitivity, i.e. the unresponsive cardiovascular system calls for a higher level of catecholamines to achieve the same effect
- Decreased renin, angiotensin and aldosterone concentrations, which is mainly due to the fall in renin activity (Tzunoda et al, 1986).
Effects of ageing on vascular structure
- Large arteries dilate. The aorta, particularly aortic root, dilates over the course of your lifetime. In the Framingham study, for every ten years of age over 16, male aortic diameter increased by 0.9mm in size-adjusted terms (Lam et al, 2010).
- All arterial walls thicken. Overall, arteries everywhere develop a larger lumen and a thicker wall, which is mainly the result of a thicker tunica intima and media.
- Decreased windkessel effect due to a loss of large vessel elasticity results in the transmission of ventricular pressure further to the more distal vessels
Effects of ageing on vascular function
- Arterial compliance decreases. The increased amount of glycosaminoglycans in the extracellular matrix, as well as the thicker arterial walls, all reduce the compliance of the arterial vascular tree.
- Endothelial vasodilation is impaired. The normal vasodilation which is mediated by nitric-oxide-mediated endothelial functions becomes impaired in old age, which basically means that resting vessel tone trends towards vasoconstriction.
- Pulmonary arterial pressure increases. Specifically, the PASP increases by 28% every 1.6 years (Lam et al, 2009). At least some of this increase must be due to the diastolic dysfunction of the left ventricle.
- Pulse pressure increases. Stiffer vessels and an earlier return of the reflected pulse wave cause the systolic pressure to rise more than the diastolic (which often stay the same).