Medical-Surgical Nursing in Canada (Section 7) - Hypertension Management PDF

CHAPTER 35...

CHAPTER 35 Nursing Management Hypertension Written by: Melissa L. Hutchinson Adapted by: Kara Sealock http://evolve.elsevier.com/Canada/Lewis/medsurg Review Questions (Online Only) Conceptual Care Map Creator Key Points Audio Glossary Answer Guidelines for Case Study Content Updates LEARNING OBJECTIVES 1. Relate the pathophysiological mechanisms associated with primary 4. Explain the collaborative care of the older adult with primary hypertension to the clinical manifestations and complications. hypertension. 2. Select appropriate strategies for the prevention of primary 5. Prioritize the nursing management of the patient with primary hypertension. hypertension. 3. Describe the collaborative care for primary hypertension, including 6. Describe the collaborative care of a patient with hypertensive crisis. drug therapy and lifestyle modifications. KEY TERMS baroreceptors, p. 790 hypertensive crisis, orthostatic hypotension, secondary hypertension, blood pressure (BP), p. 789 p. 809 p. 806 p. 793 cardiac output (CO), p. 789 isolated systolic hypertension primary (essential) systemic vascular resistance hypertension, p. 791 (ISH), p. 792 hypertension, p. 793 (SVR), p. 789 Hypertension, or high blood pressure (BP), is one of the most Cardiac output (CO) is the volume of blood ejected from important modifiable risk factors that can lead to the develop- the heart per minute. CO can be described as the stroke volume ment of cardiovascular disease (CVD). As BP increases, so (SV, or the amount of blood pumped out of the left ventricle per does the risk for myocardial infarction (MI), heart failure, stroke, beat [~70 mL]) multiplied by the heart rate (HR) for 1 minute. and renal disease. This chapter discusses the nursing and Systemic vascular resistance (SVR) is the force opposing the interprofessional care of patients who are at risk for or who movement of blood within the blood vessels. The radius of the have hypertension. small arteries and arterioles is the principal factor determining Copyright © 2018. Elsevier Canada. All rights reserved. vascular resistance. A small change in the radius of the arterioles NORMAL REGULATION OF BLOOD PRESSURE creates a major change in the SVR. If SVR is increased and CO remains constant or increases, arterial BP will increase. Blood pressure (BP) is the force exerted by the blood against The mechanisms that regulate BP can affect either CO or the walls of the blood vessel and must be adequate for tissue SVR, or both. Regulation of BP is a complex process involving perfusion to be maintained during activity and rest. The nervous, cardiovascular, renal, and endocrine functions (Figure maintenance of normal BP and tissue perfusion requires the 35-1). BP is regulated by both short-term (over seconds to hours) integration of both systemic factors and local peripheral vascular and long-term (over days to weeks) mechanisms. Short-term effects. Arterial BP is primarily a function of cardiac output mechanisms, including the effects exerted by the sympathetic (CO) and systemic vascular resistance (SVR). The relationship nervous system (SNS) and the vascular endothelium, are active between the two is summarized by the following equation: within a few seconds. Long-term mechanisms include renal Arterial blood pressure = cardiac output multiplied by systemic and hormonal processes that regulate arteriolar resistance and vascular resistance (arterial BP = CO × SVR). blood volume. 789 Lewis, S. L., Bucher, L., Heitkemper, M. M., Harding, M. M., & Harding, M. M. (2018). Medical-surgical nursing in canada - e-book. Elsevier Canada. Created from senecac on 2024-11-15 20:40:39.  790 SECTION 7 Problems of Oxygenation: Perfusion Sympathetic nervous system Cardiac a1- and a2-Adrenergic receptors Heart rate (vasoconstriction) Contractility b2-Adrenergic receptors Conductivity (vasodilation) Local regulation Vasodilators Prostaglandins Blood pressure = Cardiac output × Systemic vascular resistance Nitric oxide Vasoconstrictors Endothelin Renal fluid volume control Neurohormonal Renin-angiotensin-aldosterone Vasoconstrictors system Angiotensin Natriuretic peptides Norepinephrine FIGURE 35-1 Factors influencing blood pressure (BP). Hypertension develops when one or more of the BP-regulating mechanisms are defective. Sympathetic Nervous System standing, there is a transient decrease in BP. The vasomotor The nervous system, which reacts within seconds after a decrease centre is stimulated and activates the SNS, causing peripheral in arterial pressure, increases BP primarily by activation of the vasoconstriction and increased venous return to the heart. If SNS. Increased SNS activity increases HR and cardiac contractility, this response did not occur, there would be inadequate blood produces widespread vasoconstriction in the peripheral arterioles, flow to the brain, resulting in dizziness. Cerebral cortical per- and promotes the release of renin from the kidneys. The net ceptions such as pain and stress activate the vasomotor centres effect of SNS activation is to increase arterial pressure by increasing through the neuronal connections. both CO and SVR. Baroreceptors. Baroreceptors (pressoreceptors) are special- Changes in BP are sensed by specialized nerve cells called ized nerve cells located in the carotid sinus at the bifurcation of baroreceptors and transmitted to the vasomotor centres in the the external and internal carotid arteries and the arch of the brain stem. Information received in the brain stem is relayed aorta. They are sensitive to stretching and, when stimulated by throughout the brain by complex networks of interneurons that an increase in BP, send inhibitory impulses to the sympathetic excite or inhibit efferent nerves, thereby influencing cardiovascular vasomotor centre in the brain stem. Inhibition of sympathetic function. Sympathetic efferent nerves innervate cardiac and activity results in decreased HR, decreased force of contraction, vascular smooth muscle cells. Under normal conditions, a low and vasodilation in peripheral arterioles. Increased parasympa- level of continuous sympathetic activity maintains tonic vaso- thetic activity (vagus nerve) also reduces HR. constriction. BP may be reduced by withdrawal of SNS activity A fall in BP, sensed by the baroreceptors, leads to activation or by stimulation of the parasympathetic nervous system, which of the SNS. The result is constriction of the peripheral arterioles, decreases the HR (via the vagus nerve) and thereby decreases CO. increased HR, and increased contractility of the heart. The The neurotransmitter norepinephrine (NE) is released from baroreceptors have an important role in the maintenance of BP sympathetic nerve endings. NE activates receptors located in stability during normal activities. In the presence of longstanding the sinoatrial node, the myocardium, and vascular smooth muscle. hypertension, the baroreceptors become adjusted to elevated The response to NE depends on the type and the density of levels of BP and recognize this level as “normal.” Consequently, receptors present. SNS receptors are classified as α1, α2, β1, and the long-term regulation of arterial pressure requires activation β2 (Table 35-1). α-Adrenergic receptors located in peripheral of other mechanisms (primarily hormonal and renal) to maintain vasculature cause vasoconstriction when stimulated by NE. normal BP. The baroreceptor reflex is less responsive in some β1-Adrenergic receptors in the heart respond to NE with increased older adults. HR (chronotropic effect), increased force of contraction (inotropic effect), and increased speed of conduction (dromotropic effect). Vascular Endothelium Copyright © 2018. Elsevier Canada. All rights reserved. Diminished responsiveness of cardiovascular cells to sympathetic The vascular endothelium is a single cell layer that lines the stimulation is one of the most significant cardiovascular effects blood vessels. Previously considered inert, it is now known to of aging. The smooth muscle of the blood vessels has β1-adrenergic have the ability to produce vasoactive substances and growth and β2-adrenergic receptors. β2-Adrenergic receptors are activated factors. Nitric oxide, an endothelium-derived relaxing factor primarily by epinephrine released from the adrenal medulla and (EDRF), helps maintain low arterial tone at rest, inhibits growth cause vasodilation. of the smooth muscle layer, and inhibits platelet aggregation. The sympathetic vasomotor centre, located in the medulla, Other substances released by the vascular endothelium with local interacts with many areas of the brain to maintain normal BP vasodilator effects include prostacyclin and endothelium-derived under various conditions. During exercise, the motor area of hyperpolarizing factor. the cortex is stimulated, activating the vasomotor centre and the Endothelin (ET), produced by the endothelial cells, is an SNS through neuronal connections. This causes an appropriate extremely potent vasoconstrictor. There are three subclasses of ETs: increase in BP to accommodate the increased oxygen demand ET-1, ET-2, and ET-3. ET-1 is the most potent ET in producing of the exercising muscles. During postural change from lying to vasoconstriction. ET-1 also causes adhesion and aggregation of Lewis, S. L., Bucher, L., Heitkemper, M. M., Harding, M. M., & Harding, M. M. (2018). Medical-surgical nursing in canada - e-book. Elsevier Canada. Created from senecac on 2024-11-15 20:40:39.  CHAPTER 35 Nursing Management: Hypertension 791 TABLE 35-1 SYMPATHETIC NERVOUS and growth promotion) may contribute to atherosclerosis and SYSTEM RECEPTORS primary hypertension. Prostaglandins (PGs) E2 (PGE2) and I2 (PGI2), secreted by INFLUENCING BLOOD the renal medulla, have a vasodilator effect on the systemic PRESSURE circulation. This results in decreased SVR and lowering of BP. Adrenergic Response When (PGs are discussed in Chapter 14.) Receptor Location Activated α1 Vascular smooth muscle Vasoconstriction Endocrine System Heart Increased contractility Stimulation of the SNS results in release of epinephrine along α2 Presynaptic membrane Inhibition of with a small fraction of NE by the adrenal medulla. Epinephrine norepinephrine release increases CO by increasing HR and myocardial contractility. Vascular smooth muscle Vasoconstriction β1 Heart Increased contractility Epinephrine activates β2-adrenergic receptors in peripheral (positive inotropic arterioles of skeletal muscle, causing vasodilation. In peripheral effect) arterioles with only α1-adrenergic receptors (skin and kidneys), Increased heart rate epinephrine causes vasoconstriction. (positive chronotropic The adrenal cortex is stimulated by A-II to release aldosterone. effect) (Release of aldosterone is also regulated by other factors, such Increased conduction as low sodium levels [see Chapters 50 and 51].) Aldosterone (positive dromotropic effect) stimulates the kidneys to retain sodium and, therefore, water. Juxtaglomerular cells Increased renin This increases BP by increasing CO. secretion An increased blood sodium osmolarity level stimulates the β2 Smooth muscle of Vasodilation release of antidiuretic hormone (ADH) from the posterior peripheral blood vessels Relaxation pituitary gland. ADH increases the ECF volume by promoting in skeletal muscle, Gluconeogenesis the reabsorption of water in the distal and the collecting tubules coronary arteries, lungs, Increase in secretion kidneys, liver, islet cells, of the kidneys. The resulting increase in blood volume can cause bladder, liver an elevation in BP. Dopaminergic Primarily kidney and Vasodilation In the healthy person, these regulatory mechanisms function receptors mesenteric blood in response to the demands of the body. When hypertension vessels develops, one or more of the BP-regulating mechanisms are defective. HYPERTENSION neutrophils and stimulates smooth muscle growth. Endothelial function and dysfunction is an area of ongoing investigation. Hypertension is sustained elevation of systemic arterial BP and is There is some evidence that vascular endothelial dysfunction the leading cause for visits to primary care physicians (Hypertension may contribute to atherosclerosis and primary hypertension. The Canada, 2014). High BP is the most significant modifiable risk factor prevention or reversal of endothelial dysfunction may become for cardiovascular disease and mortality in Canada (McAlister, important for therapeutic interventions in the future. Wilkins, Joffres, et al., 2011). High blood pressure remains a sig- nificant cardiovascular risk factor affecting 40% of the global adult Renal System population ≥25 years (World Health Organization, 2013) and is pre- The kidneys contribute to BP regulation by controlling sodium dicted to become the leading cause of death and disability worldwide excretion and extracellular fluid (ECF) volume (see Chapter 47). by 2020 (Sliwa, Stewart, & Gersh, 2011). As indicated by Padwal, Sodium retention results in water retention, which causes an Bienek, McAlister, et al. (2015), even small incremental changes in increased ECF volume. This increases the venous return to the systolic and diastolic pressures have a direct effect on mortality—for heart, increasing the stroke volume, which elevates the BP through every 20-mm Hg increase in systolic BP to >115 mm Hg (or a an increase in CO. 10-mm Hg increase in diastolic BP to >75 mm Hg), the risk for The renin–angiotensin–aldosterone system (RAAS) also plays cardiovascular mortality doubles. The prevalence of diagnosed an important role in BP regulation. In response to sympathetic high BP has steadily increased among the Canadian population, stimulation, decreased blood flow through the kidneys, or from 12.9% in 1998–1999 (Dai, Robitaille, Bancej, et al., 2010) Copyright © 2018. Elsevier Canada. All rights reserved. decreased serum sodium concentration, renin is secreted from the to 22.6% in 2012–2013 (Padwal et al., 2015). Consequently, juxtaglomerular apparatus in the kidney. Renin is an enzyme that new recommendations have appeared in the 2017 Hypertension converts angiotensinogen to angiotensin I. Angiotensin-converting Canada guidelines (formerly the Canadian Hypertension Education enzyme (ACE) converts angiotensin I into angiotensin II (A-II), Program [CHEP] guidelines). CHEP is Hypertension Canada’s which can increase BP by two different mechanisms (see Chapter “knowledge translation program that targets various healthcare 47, Figure 47-6). First, A-II is a potent vasoconstrictor and professionals in clinical and community settings, provides regularly increases vascular resistance, resulting in an immediate increase updated standardized recommendations and clinical practice in BP. Second, over a period of hours or days, A-II increases BP guidelines to detect, treat and control hypertension” (Hypertension indirectly by stimulating the adrenal cortex to secrete aldosterone, Canada, 2017). which causes sodium and water retention by the kidneys, resulting Hypertension is defined as a systolic blood pressure (SBP) in increased blood volume and increased CO. equal to or greater than 140 mm Hg or a diastolic blood pressure A-II also functions at a local level within the heart and the (DBP) equal to or greater than 90 mm Hg. According to the blood vessels. The local vasoactive effects of A-II (vasoconstriction Canadian Diabetes Association (CDA) and Hypertension Canada Lewis, S. L., Bucher, L., Heitkemper, M. M., Harding, M. M., & Harding, M. M. (2018). Medical-surgical nursing in canada - e-book. Elsevier Canada. Created from senecac on 2024-11-15 20:40:39.  792 SECTION 7 Problems of Oxygenation: Perfusion TABLE 35-2 TARGET VALUES FOR BLOOD DETERMINANTS OF HEALTH PRESSURE* Hypertension Setting Target (mm Hg) Ethnicity: Education and Literacy Out-of-Office Assessments (Home or Pharmacy) 50% of all Canadians are not aware of the impact of hypertension on Home blood pressure and daytime ambulatory ≤135/85 kidneys, of the need to adhere to antihypertensive medication, and blood pressure measurement (ABPM)* that hypertension is a chronic condition. 24-hour ambulatory blood pressure