<\/p>\n
If a person is suffering from diabetes or hypertension<\/a>, he must buy a blood sugar test kit to test diabetes<\/a> and a blood pressure monitor for blood pressure<\/a>, which they can use at home.<\/p>\n People sometimes refer to hypertension as a “silent killer,” and many people do not know they have it. The American Heart Association (AHA) stresses that most of the time, there are no symptoms. People usually find out about high blood pressure when doctors take blood pressure readings or take themselves home.<\/span><\/p>\n keywords: type-1 diabetes, type-2 diabetes, gestational diabetes, Hypertension<\/p>\n Not all people with diabetes notice symptoms until they are effectively controlling their condition. If symptoms of high blood sugar levels appear, they include:<\/p>\n There are three types of diabetes, all of which have different causes:<\/p>\n Type 1 diabetes appears during childhood or adolescence, but it can occur later in life. Symptoms may emerge relatively suddenly or over several weeks. Type 1 occurs when the immune system attacks cells in the pancreas that produce insulin. There is no way to avoid type 1 diabetes.<\/p>\n Type 2 diabetes can take years to develop, and most people do not show symptoms. A person usually learns that they have diabetes or type 2 diabetes, such as neuropathy or kidney problems, by attending the screening or having diabetes. Keywords: type-1 diabetes, type-2 diabetes, gestational diabetes, Hypertension<\/span><\/p>\n Gestational diabetes occurs only in pregnancy, but it may increase the risk of type 2 diabetes later in life. If regular checkups show high blood sugar levels during pregnancy, doctors will monitor the person’s condition until delivery. They will continue to do so even after a few weeks, but blood sugar levels usually fall. Gestational diabetes can lead to various complications, including pre-eclampsia, the main symptom of which is very high blood pressure. Keywords: type-1 diabetes, type-2 diabetes, gestational diabetes, Hypertension<\/p>\n The authors of a 2012 study note that diabetes and high blood pressure often occur together and may share some common causes. Contains:<\/span><\/p>\n A person with diabetes either does not have enough insulin to process glucose or does not work effectively. Insulin is the hormone that enables the body to process glucose from food and use it as energy. As a result of insulin problems, glucose cannot enter cells to provide energy, and it accumulates in the bloodstream instead. Keywords: type-1 diabetes, type-2 diabetes, gestational diabetes, Hypertension<\/span><\/p>\n A meta-analysis seen in the Journal of the American College of Cardiology (JACC) in 2015 looked at data from more than 4 million adults. It concluded that people with high blood pressure are at greater risk of developing type 2 diabetes. This link may be due to processes occurring in the body that affect both conditions, for example, inflammation.<\/span><\/p>\n The combined effect of diabetes and hypertension can increase<\/strong> heart disease, kidney disease, and other health problems. In 2012, researchers cited data that 30% of people with type 1 diabetes and 50\u201380% of people with type 2 diabetes have high blood pressure in the United States. High glucose levels in the blood can increase blood pressure:<\/span><\/p>\n Hypertension and Diabetes also share similar risk factors. Contains: Excess weight and body fat Following an unhealthy diet Having a passive lifestyle, stress and poor sleep habits Smoking tobacco old age Low vitamin D levels<\/span><\/p>\n Drug for angina with or without hypertension :<\/li>\n ACE Inhibitors<\/strong><\/em> Renin-Angiotensin-Aldosterone System<\/strong><\/em> Renin-Angiotensin-Aldosterone System cont.<\/strong><\/p>\n \uf097 Angiotensin II is a powerful vasoconstrictor that causes a rise in peripheral resistance and increases pressure.<\/p>\n \uf097 Angiotensin II works to increase the release of aldosterone from the adrenal glands.<\/p>\n \uf097 Aldosterone causes renal retention of sodium and water, which further increases blood pressure by increasing volume. (Karch, 2012, pg. 671)<\/p>\n keywords: type-1 diabetes, type-2 diabetes, gestational diabetes, Hypertension<\/p>\n Mechanism of Action for ACE Inhibitors \uf097 ACE Inhibitors work in the lungs to inhibit Angiotensin-Converting Enzyme from turning Angiotensin I into Angiotensin II.<\/p>\n \uf097 These medications cause an increase in bradykinin, which inhibits kinase II, another name for Angiotensin-Converting Enzyme. (Lehne, 2007, pg. 464)Blood Pressure is decreased due to a decrease in blood volume, peripheral resistance, and cardiac load.<\/p>\n \uf097 ACE Inhibitors inhibit vasoconstriction and release of aldosterone, which inhibits the retention of sodium and water<\/p>\n Indications For Use:<\/strong> Indications For Use cont.<\/strong> Indications For Use cont. Indications For Use cont. Adverse Effects<\/strong> Adverse Effects cont. <\/p>\n High blood pressure (BP), or hypertension,\u00a0is defined by two levels by 2017 American College of Cardiology\/American Heart Association (ACC\/AHA) guidelines\u00a0[1<\/a>,\u00a02<\/a>]\u00a0<\/sup>: (1) elevated BP, with a systolic pressure (SBP) between 120 and 129 mm Hg and diastolic pressure (DBP) less than 80 mm Hg, and (2) stage 1 hypertension, with an SBP of 130 to 139 mm Hg or a DBP of 80 to 89 mm Hg.<\/p>\n Hypertension is the most common primary diagnosis in the United States.\u00a0[3<\/a>]\u00a0<\/sup>It affects approximately 86\u00a0million adults (\u226520 years) in the United States\u00a0[4<\/a>]\u00a0<\/sup>and is a major risk factor for stroke, myocardial infarction, vascular disease, and chronic kidney disease. See the image below.<\/p>\n Hypertension is defined as systolic blood pressure (SBP) of 140 mm Hg or more, diastolic blood pressure (DBP) of 90 mm Hg or more, or taking antihypertensive medication.\u00a0[5<\/a>]<\/sup><\/p>\n Based on recommendations of the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), the classification of BP for adults aged 18 years or older has been as follows\u00a0[5<\/a>]\u00a0<\/sup>:<\/p>\n Normal: Systolic lower than 120 mm Hg, diastolic lower than 80 mm Hg<\/p>\n<\/div>\n<\/li>\n Prehypertension: Systolic 120-139 mm Hg, diastolic 80-89 mm Hg<\/p>\n<\/div>\n<\/li>\n Stage 1: Systolic 140-159 mm Hg, diastolic 90-99 mm Hg<\/p>\n<\/div>\n<\/li>\n Stage 2: Systolic 160 mm Hg or greater, diastolic 100 mm Hg or greater<\/p>\n<\/div>\n<\/li>\n<\/ul>\n The 2017 ACC\/AHA guidelines eliminate the classification of prehypertension and divide it into two levels\u00a0[1<\/a>,\u00a02<\/a>]\u00a0<\/sup>:<\/p>\n Elevated blood pressure with systolic pressure between 120 and 129 mm Hg and diastolic pressure less than 80 mm Hg<\/p>\n<\/div>\n<\/li>\n Stage 1 hypertension, with a systolic pressure of 130 to 139 mm Hg or a diastolic pressure of 80 to 89 mm Hg<\/p>\n<\/div>\n<\/li>\n<\/ul>\n Hypertension may be primary, which may develop as a result of environmental or genetic causes, or secondary, which has multiple etiologies, including renal, vascular, and endocrine causes. Primary or essential hypertension accounts for 90-95% of adult cases, and secondary hypertension accounts for 2-10% of cases.<\/p>\n See\u00a0Presentation<\/a> for more details.<\/p>\n The evaluation of hypertension involves accurately measuring the patient\u2019s blood pressure, performing a focused medical history and physical examination, and obtaining results of routine laboratory studies.\u00a0[5<\/a>,\u00a06<\/a>]\u00a0<\/sup>A 12-lead electrocardiogram should also be obtained. These steps can help determine the following\u00a0[5<\/a>,\u00a06<\/a>,\u00a07<\/a>]\u00a0<\/sup>:<\/p>\n Presence of end-organ disease<\/p>\n<\/div>\n<\/li>\n Possible causes of hypertension<\/p>\n<\/div>\n<\/li>\n Cardiovascular risk factors<\/p>\n<\/div>\n<\/li>\n Baseline values for judging biochemical effects of therapy<\/p>\n<\/div>\n<\/li>\n<\/ul>\n Other studies may be obtained on the basis of clinical findings or in individuals with suspected secondary hypertension and\/or evidence of target-organ diseases, such as CBC, chest radiograph, uric acid, and urine microalbumin.\u00a0[5<\/a>]<\/sup><\/p>\n See\u00a0Workup<\/a> for more details.<\/p>\n Many guidelines exist for the management of hypertension. Most groups, including the JNC, the American Diabetes Associate (ADA), and the American Heart Association\/American Stroke Association (AHA\/ASA), recommend lifestyle modification as the first step in managing hypertension.<\/p>\n Lifestyle modifications<\/em><\/p>\n JNC 7 recommendations to lower BP and decrease cardiovascular disease risk include the following, with greater results achieved when 2 or more lifestyle modifications are combined\u00a0[5<\/a>]\u00a0<\/sup>:<\/p>\n Weight loss (range of approximate systolic BP reduction [SBP], 5-20 mm Hg per 10 kg)<\/p>\n<\/div>\n<\/li>\n Limit alcohol intake to no more than 1 oz (30 mL) of ethanol per day for men or 0.5 oz (15 mL) of ethanol per day for women and people of lighter weight (range of approximate SBP reduction, 2-4 mm Hg)<\/p>\n<\/div>\n<\/li>\n Reduce sodium intake to no more than 100 mmol\/day (2.4 g sodium or 6 g sodium chloride; the range of approximate SBP reduction, is 2-8 mm Hg)\u00a0[8<\/a>]<\/sup><\/p>\n<\/div>\n<\/li>\n Maintain adequate intake of dietary potassium (approximately 90 mmol\/day)<\/p>\n<\/div>\n<\/li>\n Maintain adequate intake of dietary calcium and magnesium for general health.<\/p>\n<\/div>\n<\/li>\n Stop smoking and reduce intake of dietary saturated fat and cholesterol for overall cardiovascular health.<\/p>\n<\/div>\n<\/li>\n Engage in aerobic exercise at least 30 minutes daily for most days (range of approximate SBP reduction, 4-9 mm Hg)<\/p>\n<\/div>\n<\/li>\n<\/ul>\n The AHA\/ASA recommends a low sodium diet, is high in potassium, and promotes the consumption of fruits, vegetables, and low-fat dairy products for reducing BP and lowering the risk of stroke. Other recommendations include increasing physical activity (30 minutes or more of moderate-intensity activity on a daily basis) and losing weight (for overweight and obese persons).<\/p>\n The 2018 European Society of Cardiology (ESC) and the European Society of Hypertension (ESH)\u00a0guidelines recommend a low-sodium diet (limited to 2 g per day) as well as reducing body-mass index (BMI) to 20-25 kg\/m2<\/sup>\u00a0and waist circumference (to < 94 cm in men and < 80 cm in women).\u00a0[9<\/a>]<\/sup><\/p>\n Pharmacologic therapy<\/em><\/p>\n If lifestyle modifications are insufficient to achieve the goal of BP, there are several drug options for treating and managing hypertension. Thiazide diuretics, an angiotensin-converting enzyme inhibitor (ACEI) \/angiotensin receptor blocker (ARB), or calcium channel blocker (CCB) are the preferred agents in nonblack populations, whereas CCBs or thiazide diuretics are favored in black hypertensive populations.\u00a0[10<\/a>]\u00a0<\/sup>These recommendations do not exclude the use of ACE inhibitors or ARBs in the treatment of black patients or CCBs or diuretics in non-black persons. Often, patients require several antihypertensive agents to achieve adequate BP control.<\/p>\n Compelling indications for specific agents include comorbidities such as heart failure, ischemic heart disease, chronic kidney disease, and diabetes. Drug intolerability or contraindications may also be factors.\u00a0[5<\/a>]<\/sup><\/p>\n The following are drug class recommendations for compelling indications based on various clinical trials\u00a0[5<\/a>]\u00a0<\/sup>:<\/p>\n Heart failure: Diuretic, beta-blocker, ACE inhibitor\/ARB, an aldosterone antagonist<\/p>\n<\/div>\n<\/li>\n Following myocardial infarction: Beta-blocker, ACE inhibitor.<\/p>\n<\/div>\n<\/li>\n Diabetes:\u00a0 ACE inhibitor\/ARB<\/p>\n<\/div>\n<\/li>\n Chronic kidney disease: ACE inhibitor\/ARB<\/p>\n High blood pressure, or hypertension, is the most common primary diagnosis in the United States,\u00a0[3<\/a>]. It<\/sup> is one of the most common worldwide diseases afflicting humans and is a major risk factor for stroke, myocardial infarction, and vascular and chronic kidney disease. Despite extensive research over the past several decades, the etiology of most cases of adult hypertension is still unknown, and control of blood pressure is suboptimal in the general population. Due to the associated morbidity and mortality, and cost to society, preventing and treating hypertension is an important public health challenge. Fortunately, recent advances and trials in hypertension research are leading to an increased understanding of the pathophysiology of hypertension and the promise of novel pharmacologic and interventional treatments for this widespread disease.<\/p>\n According to the American Heart Association (AHA), approximately 86 million adults (34%) in the United States are affected by hypertension, which is defined as systolic blood pressure (SBP) of 140 mm Hg or more or diastolic blood pressure (DBP) of 90 mm Hg or more, taking antihypertensive medication, or having been told by clinicians on at least 2 occasions as having hypertension.\u00a0[4<\/a>]\u00a0<\/sup>Substantial improvements have been made with regard to enhancing awareness and treatment of hypertension. However, a National Health Examination Survey (NHANES) spanning 2011-2014 revealed that 34% of US adults aged 20 years and older are hypertensive, and NHANES 2013-2014 data showed that 15.9% of these hypertensive adults are unaware they are hypertensive; these data have increased from NHANES 2005-2006 data that showed 29% of US adults aged 18 years and older were hypertensive and that 7% of these hypertensive adults had never been told that they had hypertension.\u00a0[4<\/a>]<\/sup><\/p>\n Furthermore, of those with high blood pressure (BP), 78% were aware they were hypertensive, 68% were being treated with antihypertensive agents, and only 64% of treated individuals had controlled hypertension.\u00a0[4<\/a>]\u00a0<\/sup>In addition, previous data from NHANES estimated that 52.6% (NHANES 2009-2010) to 55.8% (NHANES 1999-2000) of adults aged 20 years and older have prehypertension, defined as an untreated SBP of 120-139 mm Hg or untreated DBP of 80-89 mmHg.\u00a0[4<\/a>]\u00a0<\/sup>(See\u00a0Epidemiology<\/a>.)<\/p>\n Data from the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), which was released in 2003, were relatively similar to the NHANES data. The JNC 7 noted that approximately 30% of adults were unaware of their hypertension; up to 40% of people with hypertension were not receiving treatment; and, of those treated, up to 67% did not have their BP controlled to less than 140\/90 mm Hg.\u00a0[5<\/a>]<\/sup><\/p>\n Hypertension is the most important modifiable risk factor for coronary heart disease (the leading cause of death in North America), stroke (the third leading cause), congestive heart failure, end-stage renal disease, and peripheral vascular disease. Therefore, healthcare professionals must not only identify and treat patients with hypertension but also promote a healthy lifestyle and preventive strategies to decrease the prevalence of hypertension in the general population. (See Treatment.)<\/p>\n Defining abnormally high blood pressure (BP) is extremely difficult and arbitrary. Furthermore, the relationship between systemic arterial pressure and morbidity appears to be quantitative rather than qualitative. A level for high BP must be agreed upon in clinical practice for screening patients with hypertension and for instituting diagnostic evaluation and initiating therapy. Because the risk to an individual patient may correlate with the severity of hypertension, a classification system is essential for making decisions about the aggressiveness of treatment or therapeutic interventions. (See Presentation.)<\/p>\n Based on recommendations of the JNC 7, the classification of BP (expressed in mm Hg) for adults aged 18 years or older is as follows\u00a0[5<\/a>]\u00a0<\/sup>:<\/p>\n Normal: systolic lower than 120 mm Hg, diastolic lower than 80 mm Hg<\/p>\n<\/div>\n<\/li>\n Prehypertension: systolic 120-139 mm Hg, diastolic 80-89 mm Hg<\/p>\n<\/div>\n<\/li>\n Stage 1: systolic 140-159 mm Hg, diastolic 90-99 mm Hg<\/p>\n<\/div>\n<\/li>\n Stage 2: systolic 160 mm Hg or greater, diastolic 100 mm Hg or greater<\/p>\n<\/div>\n<\/li>\n<\/ul>\n The classification above is based on the average of 2 or more readings taken at each of 2 or more visits after initial screening.\u00a0[5<\/a>,\u00a07<\/a>]\u00a0<\/sup>Normal BP with respect to cardiovascular risk is less than 120\/80 mm Hg. However, unusually low readings should be evaluated for clinical significance.<\/p>\n Prehypertension, a new category designated in the JNC 7 report, emphasizes that patients with prehypertension are at risk for progression to hypertension and that lifestyle modification are important preventive strategy.<\/p>\n However, the 2017 ACC\/AHA guidelines eliminate the classification of prehypertension and divide it into two levels\u00a0[1<\/a>,\u00a02<\/a>]\u00a0<\/sup>: (1) elevated BP, with a systolic pressure (SBP) between 120 and 129 mm Hg and diastolic pressure (DBP) less than 80 mm Hg, and (2) stage 1 hypertension, with an SBP of 130 to 139 mm Hg or a DBP of 80 to 89 mm Hg.<\/p>\n From another perspective, hypertension may be categorized as either essential or secondary. Primary (essential) hypertension is diagnosed in the absence of an identifiable secondary cause. Approximately 90-95% of adults with hypertension have primary hypertension, whereas secondary hypertension accounts for around 5-10% of the cases.\u00a0[11<\/a>]\u00a0<\/sup>However, secondary forms of hypertension, such as primary hyperaldosteronism, account for 20% of resistant hypertension (hypertension in which BP is >140\/90 mm Hg despite the use of medications from 3 or more drug classes, 1 of which is a thiazide diuretic).<\/p>\n Especially severe cases of hypertension, or hypertensive crises, are defined as a BP of more than 180\/120 mm Hg and may be further categorized as hypertensive emergencies or urgencies. Hypertensive emergencies are characterized by evidence of impending or progressive target organ dysfunction, whereas hypertensive urgencies are those situations without progressive target organ dysfunction.\u00a0[5<\/a>]<\/sup><\/p>\n In hypertensive emergencies, the BP should be aggressively lowered within minutes to an hour by no more than 25% and then lowered to 160\/100-110 mm Hg within the next 2-6 hours.\u00a0[5<\/a>]\u00a0<\/sup>Acute end-organ damage in the setting of a hypertensive emergency may include the following\u00a0[12<\/a>]\u00a0<\/sup>:<\/p>\n Neurologic: hypertensive encephalopathy, cerebral vascular accident\/cerebral infarction, subarachnoid hemorrhage, intracranial hemorrhage<\/p>\n<\/div>\n<\/li>\n![\"\"](\"https:\/\/i0.wp.com\/www.diabetesasia.org\/magazine\/wp-content\/uploads\/2020\/01\/BP.png?resize=379%2C252&ssl=1\")
<\/a><\/p>\nHow to test Hypertension and Diabetes at home?<\/h2>\n
How To Identify Hypertension?<\/h2>\n
How to Identify Diabetes?<\/h2>\n
\n
Type 1 Diabetes<\/h2>\n
Type2 Diabetes<\/h2>\n
Gestational Diabetes<\/h2>\n
What is the similarity between diabetes and hypertension? <\/span><\/h2>\n
\n
Can diabetes cause high blood pressure? <\/span><\/h2>\n
Can high blood pressure cause diabetes? <\/span><\/h2>\n
What are the Complications of diabetes and hypertension?<\/span><\/h2>\n
\n
\nWhat is the risk of Hypertension and type 2 diabetes?<\/span><\/h2>\n
\nThis systematic review of double-blind studies involving head-to-head comparison of antianginal drugs,
\nwas performed between January and March 2018, on articles written in English over the past 50 years
\ni.e., 72 studies in total.
\nDespite the paucity of data comparing the efficacy of anti-anginal drugs, taken all together, in none of
\nthe studies were there evidence that one drug was superior to another in the treatment of angina or to
\nprolong total exercise duration.
\nBased on these findings, the authors conclude that \u201cThe medical therapy of angina should be
\npersonalized and tailored towards the individual with an understanding of the likely
\npathophysiological mechanisms and co-morbidities.\u201d
\nThese results are clearly in line with the recommendations of the Indian Consensus on Optimal Treatment
\nof Angina (published a few days back in JAPI- November 2018):
\n\u2022 For angina patients with varying co-morbidities (diabetes, low heart rate, Hypotension, micro
\nvascular angina, LVD, or peripheral arterial disease), early addition of metabolic modulators
\nsuch as Trimetazidine is beneficial.
\n\u2022 For angina patients with varying co-morbidities (LVSD, high heart rate, hypotension, micro
\nvascular angina, peripheral arterial disease, hyperthyroidism, & COPD), early addition of
\nivabradine to B-blockers provides significant benefits.
\nI am sure, with such impactful publications, you would pass on the benefits of FLAVEDON MR &
\nCORALINE (Ivabradine) to your angina patients, as 38% of the studies retained in this meta-analysis concerned trimetazidine and\/or ivabradine. keywords: type-1 diabetes, type-2 diabetes, gestational diabetes, Hypertension<\/li>\n<\/ul>\n
\n\uf097 ACE Inhibitors are medications that belong in the class of medications known as antihypertensive medications.
\n\uf097 ACE Inhibitors work on the renin-angiotensin-aldosterone system.<\/p>\n
\n\uf097 A system that works to increase blood pressure when the pressure within the kidneys drops.
\n\uf097 As a result of low blood pressure and\/or oxygenation in the nephron, renin is released from the juxtaglomerular cells.
\n\uf097 Renin travels to the liver via the cardiovascular system and combines with angiotensinogen to form angiotensin I.
\n\uf097 Angiotensin I travels through the cardiovascular system and arrives at the lungs, changing into Angiotensin II.
\n\uf097 The alveoli use Angiotensin-Converting Enzyme, also known as kinase II to cause this conversion.
\n(Karch, 2012, pg. 671)<\/p>\n
\n\uf097 Hypertension especially for malignant
\nhypertension and hypertension secondary to renal
\narterial stenosis.
\n\uf097 Benefits of Using an ACE Inhibitor
\n\uf097 Do not interfere with cardiovascular reflexes
\n\uf097 Do not interfere with patients who have asthma-like beta-blockers
\n\uf097 Do not decrease potassium levels.
\n\uf097 Do not cause lethargy, weakness, and sexual dysfunction.
\n\uf097 \u201cACE inhibitors reduce the risk of cardiovascular mortality
\ncaused by hypertension.\u201d (Lehne,2007, pg. 465)<\/p>\n
\n\uf097 Heart Failure
\n\uf097 By decreasing the arteriolar tone, the region of blood flow to the heart improves.
\n\uf097 By decreasing afterload, cardiac output increases.
\n\uf097 Venous dilation increases, causing a decrease in pulmonary congestion and peripheral edema.
\n\uf097 It dilates the vessels of the kidneys, increasing renal flow, and helping to excrete sodium and water. This helps to decrease
\nedema and blood volume.
\n\uf097 It prevents pathologic changes in the heart that result from reducing the angiotensin II levels in the heart.
\n(Lehne, 2007, pg. 465)<\/p>\n
\n\uf097 Myocardial Infarction (MI)
\n\uf097 Decreases the chance of heart failure after an MI.
\n\uf097 Should be given for 6 weeks post-MI. If heart failure occurs, it should be considered for permanent use.
\n\uf097 Nephropathy
\n\uf097 Slows renal disease of diabetic or nondiabetic origins
\n\uf097 Decreases glomerular filtration pressure.<\/p>\n
\n\uf097 Type 2 Diabetes
\n\uf097 Decreases morbidity in high-risk patients.
\n\uf097 Increased levels of angiotensin II correlate to type 2
\ndiabetes.
\n\uf097 ACE inhibitors increase kinin levels, which increase the production of prostaglandins and nitric oxide.
\n\uf097 Prostaglandins and nitric oxide improve muscular insulin sensitivity. (Solski & Longyhore, 2008, pg. 936)
\n\uf097 May preserve pancreatic function and prevent the onset of diabetes, especially in people who have hypertension.<\/p>\n
\n\uf097 First-Dose Hypotension
\n\uf097 It usually occurs with the initial dose.
\n\uf097 Worse in patients with severe hypertension, who are on diuretics, or who are sodium or volume-depleted.
\n\uf097 Cough
\n\uf097 \u201cPersistent, dry, irritating, nonproductive cough can develop with all ACE inhibitors.\u201d (Lehne, 2007, pg. 466)
\n\uf097 Due to the rise in bradykinin which occurs due to inhibition of kinase II.
\n\uf097 Occurs in 5-10% of patients and is more common in women and the elderly<\/p>\n
\n\uf097 Hyperkalemia
\n\uf097 Potassium levels rise due to the inhibition of aldosterone, which causes potassium to be retained by the
\nkidneys.
\n\uf097 Renal Failure
\n\uf097 It can cause renal insufficiency in people with bilateral renal artery stenosis because dropping the pressure in the
\nrenal arteries in these patients can cause glomerular filtration to fail.
\n\uf097 Fetal Injury
\n\uf097 In the second and third trimesters, a fetus can experience hypotension, hyperkalemia, skull hypoplasia, renal
\nfailure, and death.
\nDrug Interactions<\/strong>
\n\uf097 Antihypertensive agents
\n\uf097 Can cause an increased effect of medications, especially with diuretics.
\n\uf097 Potassium increasing medications
\n\uf097 Cause an increased risk of hyperkalemia due to the suppression of aldosterone.
\n\uf097 Lithium
\n\uf097 Increases the risk of lithium toxicity.
\n\uf097 Allopurinol
\n\uf097 Increases hypersensitivity to the medication
\n\uf097 NSAIDs
\n\uf097 Reduce the antihypertensive effects of medication.
\nNursing Considerations
\n\uf097 Encourage lifestyle changes
\n\uf097 Weight loss
\n\uf097 Quit smoking
\n\uf097 Decrease alcohol intake
\n\uf097 Encourage exercise to help lower blood pressure
\n\uf097 Monitor Renal Function
\n\uf097 BUN, Creatinine, and Potassium levels
\n\uf097 Monitor for decreased fluid volume, which can bottom our
\nblood pressure
\n\uf097 Excessive sweating
\n\uf097 Diarrhea
\n\uf097 Vomiting
\n\uf097 Dehydration
\nNursing Considerations cont.
\n\uf097 Monitor for 1st
\n-dose hypotension
\n\uf097 May have to stop other antihypertensive medications at the initiation of
\nACE inhibitors.
\n\uf097 I may have to give these medications in lower doses in the future.
\n\uf097 Discontinue diuretics for 2-3 days before starting an ACE inhibitor.
\n\uf097 Monitor BP for several hours, and if the patient becomes hypotensive, lay
\npatient supine and consider discussing an IV bolus of saline with the
\nMD.
\n\uf097 Educate Patient
\n\uf097 Teach the patient about the medication, including the name adverse
\neffects, drug interactions.
\n\uf097 Teach the patient about the signs of hypotension, hyperkalemia, and
\nrenal failure. If the patient is taking lithium, discuss the signs of lithium
\ntoxicity.
\nTest Questions
\n1. Which of these patients would most likely be treated
\nwith an ACE inhibitor?
\na) A 38-year-old woman who has become hypertensive in
\nthe last trimester of her pregnancy.
\nb) A 78-year-old man who just had a heart attack and is in
\nrenal failure.
\nc) A 60-year-old man who has diabetes and suffers from
\nhypertension.
\nd) A 72-year-old female with a history of hypertension
\ncomes to the ER in septic shock.
\nTest Questions
\n2. Which statement by a patient taking ACE inhibitors
\ndemonstrates the patient\u2019s understanding of the
\nmedication?
\na) \u201cI don\u2019t need to exercise because the medication will
\nmake me better.\u201d
\nb) \u201cIf I feel weak or faint, I should take my
\nmedication because it will make me feel better.\u201d
\nc) \u201cI can use salt substitutes instead of the real thing.\u201d
\nd) \u201cIf I develop a cough that does not go away, I should
\ncall my doctor.\u201d
\nTest Questions
\n1. Which of these lab values would be a
\ncontraindication for taking an ACE inhibitor?
\na) Potassium 3.3
\nb) Potassium 5.6
\nc) BUN 10
\nd) Creatinine 1.2
\nTest Answers with Rationale
\n1. c is the correct answer. a, b, and d all have
\ncontraindications for giving an ACE inhibitor.
\n2. d is the correct answer. A is wrong because exercise
\nshould be encouraged. Bi’s wrong because weakness
\nand syncope are signs that the patient may be
\nhypotensive. C is wrong because salt substitutes are
\nhigh in potassium and should be used with caution
\nin patients with ACE inhibitors.
\n3. a is the right answer. Hyperkalemia is a
\ncontraindication for ACE inhibitors.
\nReferences
\n\uf097 Karch, A. (2011). Focus on nursing pharmacology (5th
\ned.). Philadephia, PA: Wolters Kluwer | Lippincott
\nWilliams & Wilkins.
\n\uf097 Lehne, R. (2007). Pharmacology for nursing care (6th ed.).
\nSt. Louis, MO: Saunders|Elsevier.
\n\uf097 Solski, L. V. & Longyhore. (2008). Prevention of type 2
\nDiabetes mellitus with angiotensin-converting enzyme inhibitors. American Journal of HealthSystem Pharmacy, 65(10): 935-40.
\n\uf097 Waterfield, J. (2008). ACE inhibitors: use, action, and
\nprescribing rationale. Nurse Prescribing, 6(3): 110-4<\/p>\nPractice Essentials<\/h2>\n
![\"Hypertension.](\"https:\/\/i0.wp.com\/img.medscapestatic.com\/pi\/meds\/ckb\/25\/37725tn.jpg?w=640&ssl=1\")
<\/a>Hypertension. Anteroposterior x-ray from a 28-year-old woman who presented with congestive heart failure secondary to her chronic hypertension or high blood pressure. The enlarged cardiac silhouette in this image is due to congestive heart failure due to the effects of chronic high blood pressure on the left ventricle. The heart then becomes enlarged, and fluid accumulates in the lungs, known as pulmonary congestion.<\/span><\/p>\nSigns and symptoms of hypertension<\/h3>\n
\n
\n
Diagnosis of hypertension<\/h3>\n
\n
Management of hypertension<\/h3>\n
\n
\n
Background<\/h2>\n
Definition and classification<\/h3>\n
\n
\n