202430 EHR519 Week 3 lecture 1 hypertension V2 GB.pdf

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Warning This material has been produced and communicated to you by or on behalf of Charles Sturt University in accordance with section 113P of the copyright act (Act). The material in this communication may by subject to copyright under the act. Any further reproduction or communication of this material by you may be the subject of copyright protection under this act. Do not remove this notice 1  Week 3: Hypertension M Schultz 2017 EHR519 week 3 Lecture 1 Dr Gavin Buzza 2  Learning Outcomes On successful completion of this topic, you should: be able to explain the pathophysiology of hypertension as it relates to cardiovascular disease and exercise physiology; be able to outline the risk factors, complications and co-morbidities that must be accounted for when applying exercise interventions to individuals with hypertension. be able to describe the effects of commonly prescribed medications on acute and chronic exercise responses that must be accounted for when applying exercise interventions to individuals with hypertension; be able to explain the diagnostic techniques and treatment procedures used in the treatment of hypertension; be able to demonstrate the ability to conduct exercise/fitness/functional tests on individuals with hypertension; and, be able to prescribe exercise as a therapeutic modality for these individuals. 3 Overview 1. Pathology and Pathophysiology of Hypertension 2. Medications to treat Hypertension 3. Considerations and Contraindications a) Testing i. BP assessments ii. Exercise testing b) Prescription i. Recommendations and procedures ii. Physiological rationale 4  Hypertension the silent killer! Often referred to as the silent killer as most patients do not have specific symptoms related to their high BP The most common, costly and modifiable cardiovascular disease (CVD) risk factor The lifetime risk of developing hypertension is 90% One in five people with elevated BP will develop the condition within 4 years Increasing age of the population (baby boomers) Lifestyle factors play a large contribution to the management of hypertension 5 Definition and Classification Blood pressure down under. Horne, et al. (2018) Classification is based on the average of two or more properly measured, seated BP readings on each of two or more office visits CVD doubles for every increment increase in SBP of 20mmHg or DBP of 10 mmHg above 115/75 mmHg 6  Other descriptive terms: Secondary or inessential = HT with known cause Isolated systolic HT (SBP of ≥140 mmHg & DBP 140 mmHg) 7 Pathophysiology 8  Blood Pressure (BP) BP: Force that the blood exerts against a vessel wall Flow: amount of blood flowing through an organ tissue or blood vessel in a given time (i.e. ml/min). Total flow (Q) = approximately 5L/min Perfusion: flow per given volume of mass of tissue (ml.min.g) Hemodynamics – physical principles of blood flow and are based on pressure and resistance F ∝ ∆P/R 9  Blood Pressure (BP) Systolic BP: peak arterial BP attained during ventricular contraction Diastolic BP: minimum arterial BP occurring during the ventricular relaxation between each cardiac cycle Difference between SBP and DBP = Pulse Pressure (PP) The force that drives blood circulation / maximum stress exerted on small arteries Mean Arterial Pressure (MAP): mean pressure from several intervals (e.g 0.1 second) throughout the cardiac cycle. Low-pressure diastole lasts longer than the high-pressure systole Estimate obtained by adding diastolic pressure and 1/3 of PP E.g. BP of 120/75 = MAP ≈ 90 mm Hg (75 + 45/3) Typical for vessels at heart level, influenced by gravity e.g. standing adult ~ 62 mm Hg at the head and 180 mm Hg in the ankle High MAP increases risk of atherosclerosis, kidney failure, aneurysm Stiff arteries causes the heart to work harder = left ventricular hypertrophy Elastic arteries absorb and store potential energy; then exert that pressure on the blood to maintain blood flow throughout the cardiac cycle (reducing stress on the smaller arteries) MAP = cardiac output x total vascular resistance 10  Peripheral Resistance is opposition to blood flow moving away from the heart. Moving blood would exert no pressure against a vessel wall unless it encountered at least some downstream resistance. Pressure and resistance are not independent variables in blood flow— rather, pressure is affected by resistance and flow is affected by both. Resistance, in turn, hinges on three variables: blood viscosity, vessel length, and vessel radius. Blood Viscosity: due to factors such as erythrocyte count, albumin concentration and dehydration. Vessel Length: i.e the farther a liquid travels through a tube, the more cumulative friction it encounters; pressure and flow therefore decline with distance. Vessel Radius: Primary method of controlling peripheral resistance from moment to moment are vasoconstriction and vasodilation (vasomotion) 11  Regulation of Blood Pressure Local, neural and hormonal control Short-term regulation of BP Sympathetic nervous system Baroreceptors in aorta and carotid arteries – Increase in BP = decreased SNS activity – Decrease in BP = increased SNS activity Long-term regulation of BP Kidneys – Via control of blood volume – Aldosterone, angiotensin II and antidiuretic hormone 12  Pathophysiology – Primary Hypertension BP is multifaceted and complicated by the network of systems that contribute towards its regulation Renal, endocrine, vascular, peripheral, central adrenergic systems Mean Arterial Pressure (MAP) = cardiac output (Q) x total peripheral resistance (TPR) Initial stages due to Progression sympathetic + ED and overactivity LVH 13  Pathophysiology of Hypertension Most individuals with essential hypertension have a normal cardiac output but a raised peripheral resistance. Peripheral resistance is not determined by large arteries or capillaries but rather small arterioles (which contain smooth muscle cells) Contraction of smooth muscle cells = rise in intracellular calcium concentration, Explains vasodilatory effect of drugs that block the calcium channels Prolonged smooth muscle constriction is thought to induce structural changes with thickening of the arteriolar vessel walls possibly mediated by angiotensin, leading to an irreversible rise in peripheral resistance Increased systemic vascular resistance, increased vascular stiffness, and increased vascular responsiveness to stimuli are central to the pathophysiology of hypertension (Foex & Sear, 2004) 14  Endothelial Dysfunction Dysfunction of the endothelium has been implicated in human essential hypertension Vascular endothelial cells play a key role in cardiovascular regulation by producing a number of potent local vasoactive agents Nitric oxide and the vasoconstrictor peptide endothelin NO mediates the vasodilatation produced by acetylcholine, bradykinin, sodium nitroprusside and nitrates. In hypertensive patients, endothelial-derived relaxation is inhibited Endothelium synthesizes endothelins, the most powerful vasoconstrictors Sensitivity to endothelin-1 is no different in hypertensive and normotensive subjects. But the vascular effects of endogenous endothelin-1 may be accentuated by reduced NO caused by hypertensive endothelial dysfunction 15  Vasoactive substances Other vasoactive systems and mechanisms affecting sodium transport and vascular tone are involved in the maintenance of a normal BP Bradykinin: a potent vasodilator that is inactivated by angiotensin converting enzyme. Thus, ACE inhibitors may exert some of their effect by blocking bradykinin inactivation Endothelin (recently discovered) = powerful, vascular, endothelial vasoconstrictor May produce a salt sensitive rise in BP Activates local renin-angiotensin systems Atrial natriuretic peptide - hormone secreted from the atria in response to blood volume Breevers et al. 2001 BMJ Produces natriuresis, diuresis and modest decrease in BP, while decreasing plasma renin and aldosterone ANP concentrations increase with increased filling pressures (atria secrets ANP) in patients with arterial hypertension and left ventricular hypertrophy 16  Hypercoagulability Those with HT have ED or damage, abnormal blood constituents (haemostatic factors, platelet activation, and fibrinolysis), and blood flow (rheology, viscosity, and flow reserve), suggesting that hypertension confers a prothrombotic or hypercoagulable state Appear to be related to target organ damage and long-term prognosis, and some may be altered by antihypertensive treatment Breevers et al. 2001 BMJ17  Autonomic Nervous System Often those with HT have increased release of, and enhanced peripheral sensitivity to norepinephrine Increased responsiveness to stressful stimuli Another feature of arterial hypertension is a resetting of the baroreflexes and decreased baroreceptor sensitivity Linked to the renin-angiotensin system 18 Pathophysiology – Secondary Hypertension Small percentage of cases Renal Sodium and fluids in the kidneys leading to volume expansion or an alteration in renal secretion of vasoactive materials that results in systemic if local changes in arteriolar tone Endocrine Abnormality of the adrenal glands 19 Renin-angiotensin system Renin is secreted from the juxtaglomerular apparatus of the kidney in response to glomerular under perfusion or a reduced salt intake. It is also released in response to stimulation from the sympathetic nervous system Responsible for converting renin substrate (angiotensinogen) to angiotensin I, a physiologically inactive substance which is rapidly converted to angiotensin II in the lungs by angiotensin converting enzyme (ACE) Angiotensin II is a potent vasoconstrictor and thus causes a rise in BP Stimulates the release of aldosterone from the zona glomerulosa of the adrenal gland, which results in a further rise in blood pressure related to sodium and water retention Beevers, Lip and O’Brien, BMJ 2001 Co-morbidities Untreated HT causes further ED damage and atherosclerotic progression, which further promotes atherosclerosis … It’s a harsh reciprocal cycle! Additional deleterious outcomes include: ✓ Hypertrophic dilated cardiomyopathy ✓ Compromised ventricular ejection and cardiac output ✓ Chronic heart failure ✓ Heart valve defects ✓ End-stage renal disease ✓ Myocardial infarction ✓ Stroke ✓ Aneurysm 22  Coronary Heart Disease In young, healthy population groups… Pulse pressure generated by the LV is relatively low and the waves reflected by the peripheral vasculature occur mainly after the end of systole, Increasing pressure during the early part of diastole and improving coronary perfusion. With ageing…. Stiffening of the aorta and elastic arteries increases the pulse pressure. Reflected waves move from early diastole to late systole. Increase in left ventricular afterload, and contributes to LVH. The widening of the pulse pressure with ageing is a strong predictor of coronary heart disease. 23  Coronary Heart Disease SP = Aortic Systolic Pressure (max aortic pressure; high pressure = high CV load) PP = Aortic Pulse Pressure (height of aortic pulse pressure; high pressure predicts CV events) AP Aortic Augmentation Pressure (diff between the 2 aortic peaks during systole; wave reflection back from the body) = magnitude & speed of reflection; indicator of arterial stiffness Aix = Augmentation index (%) = ratio of AP to PP. High pressure = stiff arteries, organ damage AIx 75 = Aix normalised to a HR of 75bpm 24