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Newly diagnosed hypertension: case study

Angela Brown

Trainee Advanced Nurse Practitioner, East Belfast GP Federation, Northern Ireland

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The role of an advanced nurse practitioner encompasses the assessment, diagnosis and treatment of a range of conditions. This case study presents a patient with newly diagnosed hypertension. It demonstrates effective history taking, physical examination, differential diagnoses and the shared decision making which occurred between the patient and the professional. It is widely acknowledged that adherence to medications is poor in long-term conditions, such as hypertension, but using a concordant approach in practice can optimise patient outcomes. This case study outlines a concordant approach to consultations in clinical practice which can enhance adherence in long-term conditions.

Hypertension is a worldwide problem with substantial consequences ( Fisher and Curfman, 2018 ). It is a progressive condition ( Jamison, 2006 ) requiring lifelong management with pharmacological treatments and lifestyle adjustments. However, adopting these lifestyle changes can be notoriously difficult to implement and sustain ( Fisher and Curfman, 2018 ) and non-adherence to chronic medication regimens is extremely common ( Abegaz et al, 2017 ). This is also recognised by the National Institute for Health and Care Excellence (NICE) (2009) which estimates that between 33.3% and 50% of medications are not taken as recommended. Abegaz et al (2017) furthered this by claiming 83.7% of people with uncontrolled hypertension do not take medications as prescribed. However, leaving hypertension untreated or uncontrolled is the single largest cause of cardiovascular disease ( Fisher and Curfman, 2018 ). Therefore, better adherence to medications is associated with better outcomes ( World Health Organization, 2003 ) in terms of reducing the financial burden associated with the disease process on the health service, improving outcomes for patients ( Chakrabarti, 2014 ) and increasing job satisfaction for professionals ( McKinnon, 2013 ). Therefore, at a time when growing numbers of patients are presenting with hypertension, health professionals must adopt a concordant approach from the initial consultation to optimise adherence.

Great emphasis is placed on optimising adherence to medications ( NICE, 2009 ), but the meaning of the term ‘adherence’ is not clear and it is sometimes used interchangeably with compliance and concordance ( De Mauri et al, 2022 ), although they are not synonyms. Compliance is an outdated term alluding to paternalism, obedience and passivity from the patient ( Rae, 2021 ), whereby the patient's behaviour must conform to the health professional's recommendations. Adherence is defined as ‘the extent to which a person's behaviour, taking medication, following a diet and/or executing lifestyle changes, corresponds with agreed recommendations from a health care provider’ ( Chakrabarti, 2014 ). This term is preferred over compliance as it is less paternalistic ( Rae, 2021 ), as the patient is included in the decision-making process and has agreed to the treatment plan. While it is not yet widely embraced or used in practice ( Fawcett, 2020 ), concordance is recognised, not as a behaviour ( Rae, 2021 ) but more an approach or method which focuses on the equal partnership between patient and professional ( McKinnon, 2013 ) and enables effective and agreed treatment plans.

NICE last reviewed its guidance on medication adherence in 2019 and did not replace adherence with concordance within this. This supports the theory that adherence is an outcome of good concordance and the two are not synonyms. NICE (2009) guidelines, which are still valid, show evidence of concordant principles to maximise adherence. Integrating the theoretical principles of concordance into this case study demonstrates how the trainee advanced nurse practitioner aimed to individualise patient-centred care and improve health outcomes through optimising adherence.

Patient introduction and assessment

Jane (a pseudonym has been used to protect the patient's anonymity; Nursing and Midwifery Council (NMC) 2018 ), is a 45-year-old woman who had been referred to the surgery following an attendance at an emergency department. Jane had been role-playing as a patient as part of a teaching session for health professionals when it was noted that her blood pressure was significantly elevated at 170/88 mmHg. She had no other symptoms. Following an initial assessment at the emergency department, Jane was advised to contact her GP surgery for review and follow up. Nazarko (2021) recognised that it is common for individuals with high blood pressure to be asymptomatic, contributing to this being referred to as the ‘silent killer’. Hypertension is generally only detected through opportunistic checking of blood pressure, as seen in Jane's case, which is why adults over the age of 40 years are offered a blood pressure check every 5 years ( Bostock-Cox, 2013 ).

Consultation

Jane presented for a consultation at the surgery. Green (2015) advocates using a model to provide a structured approach to consultations which ensures quality and safety, and improves time management. Young et al (2009) claimed that no single consultation model is perfect, and Diamond-Fox (2021) suggested that, with experience, professionals can combine models to optimise consultation outcomes. Therefore, to effectively consult with Jane and to adapt to her individual personality, different models were intertwined to provide better person-centred care.

The Calgary–Cambridge model is the only consultation model that places emphasis on initiating the session, despite it being recognised that if a consultation gets off to a bad start this can interfere throughout ( Young et al, 2009 ). Being prepared for the consultation is key. Before Jane's consultation, the environment was checked to minimise interruptions, ensuring privacy and dignity ( Green, 2015 ; NMC, 2018 ), the seating arrangements optimised to aid good body language and communication ( Diamond-Fox, 2021 ) and her records were viewed to give some background information to help set the scene and develop a rapport ( Young et al, 2009 ). Being adequately prepared builds the patient's trust and confidence in the professional ( Donnelly and Martin, 2016 ) but equally viewing patient information can lead to the professional forming preconceived ideas ( Donnelly and Martin, 2016 ). Therefore, care was taken by the trainee advanced nurse practitioner to remain open-minded.

During Jane's consultation, a thorough clinical history was taken ( Table 1 ). History taking is common to all consultation models and involves gathering important information ( Diamond-Fox, 2021 ). History-taking needs to be an effective ( Bostock-Cox, 2019 ), holistic process ( Harper and Ajao, 2010 ) in order to be thorough, safe ( Diamond-Fox, 2021 ) and aid in an accurate diagnosis. The key skill for taking history is listening and observing the patient ( Harper and Ajao, 2010 ). Sir William Osler said:‘listen to the patient as they are telling you the diagnosis’, but Knott and Tidy (2021) suggested that patients are barely given 20 seconds before being interrupted, after which they withdraw and do not offer any new information ( Demosthenous, 2017 ). Using this guidance, Jane was given the ‘golden minute’ allowing her to tell her ‘story’ without being interrupted ( Green, 2015 ). This not only showed respect ( Ingram, 2017 ) but interest in the patient and their concerns.

Once Jane shared her story, it was important for the trainee advanced nurse practitioner to guide the questioning ( Green 2015 ). This was achieved using a structured approach to take Jane's history, which optimised efficiency and effectiveness, and ensured that pertinent information was not omitted ( Young et al, 2009 ). Thomas and Monaghan (2014) set out clear headings for this purpose. These included:

• The presenting complaint
• Past medical history
• Drug history
• Social history
• Family history.

McPhillips et al (2021) also emphasised a need for a systemic enquiry of the other body systems to ensure nothing is missed. From taking this history it was discovered that Jane had been feeling well with no associated symptoms or red flags. A blood pressure reading showed that her blood pressure was elevated. Jane had no past medical history or allergies. She was not taking any medications, including prescribed, over the counter, herbal or recreational. Jane confirmed that she did not drink alcohol or smoke. There was no family history to note, which is important to clarify as a genetic link to hypertension could account for 30–50% of cases ( Nazarko, 2021 ). The information gathered was summarised back to Jane, showing good practice ( McPhillips et al, 2021 ), and Jane was able to clarify salient or missing points. Green (2015) suggested that optimising the patient's involvement in this way in the consultation makes her feel listened to which enhances patient satisfaction, develops a therapeutic relationship and demonstrates concordance.

During history taking it is important to explore the patient's ideas, concerns and expectations. Moulton (2007) refers to these as the ‘holy trinity’ and central to upholding person-centredness ( Matthys et al, 2009 ). Giving Jane time to discuss her ideas, concerns and expectations allowed the trainee advanced nurse practitioner to understand that she was concerned about her risk of a stroke and heart attack, and worried about the implications of hypertension on her already stressful job. Using ideas, concerns and expectations helped to understand Jane's experience, attitudes and perceptions, which ultimately will impact on her health behaviours and whether engagement in treatment options is likely ( James and Holloway, 2020 ). Establishing Jane's views demonstrated that she was eager to engage and manage her blood pressure more effectively.

Vincer and Kaufman (2017) demonstrated, through their case study, that a failure to ask their patient's viewpoint at the initial consultation meant a delay in engagement with treatment. They recognised that this delay could have been avoided with the use of additional strategies had ideas, concerns and expectations been implemented. Failure to implement ideas, concerns and expectations is also associated with reattendance or the patient seeking second opinions ( Green, 2015 ) but more positively, when ideas, concerns and expectations is implemented, it can reduce the number of prescriptions while sustaining patient satisfaction ( Matthys et al, 2009 ).

Physical examination

Once a comprehensive history was taken, a physical examination was undertaken to supplement this information ( Nuttall and Rutt-Howard, 2016 ). A physical examination of all the body systems is not required ( Diamond-Fox, 2021 ) as this would be extremely time consuming, but the trainee advanced nurse practitioner needed to carefully select which systems to examine and use good examination technique to yield a correct diagnosis ( Knott and Tidy, 2021 ). With informed consent, clinical observations were recorded along with a full cardiovascular examination. The only abnormality discovered was Jane's blood pressure which was 164/90 mmHg, which could suggest stage 2 hypertension ( NICE, 2019 ; 2022 ). However, it is the trainee advanced nurse practitioner's role to use a hypothetico-deductive approach to arrive at a diagnosis. This requires synthesising all the information from the history taking and physical examination to formulate differential diagnoses ( Green, 2015 ) from which to confirm or refute before arriving at a final diagnosis ( Barratt, 2018 ).

Differential diagnosis

Hypertension can be triggered by secondary causes such as certain drugs (non-steroidal anti-inflammatory drugs, steroids, decongestants, sodium-containing medications or combined oral contraception), foods (liquorice, alcohol or caffeine; Jamison, 2006 ), physiological response (pain, anxiety or stress) or pre-eclampsia ( Jamison, 2006 ; Schroeder, 2017 ). However, Jane had clarified that these were not contributing factors. Other potential differentials which could not be ruled out were the white-coat syndrome, renal disease or hyperthyroidism ( Schroeder, 2017 ). Further tests were required, which included bloods, urine albumin creatinine ratio, electrocardiogram and home blood pressure monitoring, to ensure a correct diagnosis and identify any target organ damage.

Joint decision making

At this point, the trainee advanced nurse practitioner needed to share their knowledge in a meaningful way to enable the patient to participate with and be involved in making decisions about their care ( Rostoft et al, 2021 ). Not all patients wish to be involved in decision making ( Hobden, 2006 ) and this must be respected ( NMC, 2018 ). However, engaging patients in partnership working improves health outcomes ( McKinnon, 2013 ). Explaining the options available requires skill so as not to make the professional seem incompetent and to ensure the patient continues to feel safe ( Rostoft et al, 2021 ).

Information supported by the NICE guidelines was shared with Jane. These guidelines advocated that in order to confirm a diagnosis of hypertension, a clinic blood pressure reading of 140/90 mmHg or higher was required, with either an ambulatory or home blood pressure monitoring result of 135/85 mmHg or higher ( NICE, 2019 ; 2022 ). However, the results from a new retrospective study suggested that the use of home blood pressure monitoring is failing to detect ‘non-dippers’ or ‘reverse dippers’ ( Armitage et al, 2023 ). These are patients whose blood pressure fails to fall during their nighttime sleep. This places them at greater risk of cardiovascular disease and misdiagnosis if home blood pressure monitors are used, but ambulatory blood pressure monitors are less frequently used in primary care and therefore home blood pressure monitors appear to be the new norm ( Armitage et al, 2023 ).

Having discussed this with Jane she was keen to engage with home blood pressure monitoring in order to confirm the potential diagnosis, as starting a medication without a true diagnosis of hypertension could potentially cause harm ( Jamison, 2006 ). An accurate blood pressure measurement is needed to prevent misdiagnosis and unnecessary therapy ( Jamison, 2006 ) and this is dependent on reliable and calibrated equipment and competency in performing the task ( Bostock-Cox, 2013 ). Therefore, Jane was given education and training to ensure the validity and reliability of her blood pressure readings.

For Jane, this consultation was the ideal time to offer health promotion advice ( Green, 2015 ) as she was particularly worried about her elevated blood pressure. Offering health promotion advice is a way of caring, showing support and empowerment ( Ingram, 2017 ). Therefore, Jane was provided with information on a healthy diet, the reduction of salt intake, weight loss, exercise and continuing to abstain from smoking and alcohol ( Williams, 2013 ). These were all modifiable factors which Jane could implement straight away to reduce her blood pressure.

Safety netting

The final stage and bringing this consultation to a close was based on the fourth stage of Neighbour's (1987) model, which is safety netting. Safety netting identifies appropriate follow up and gives details to the patient on what to do if their condition changes ( Weiss, 2019 ). It is important that the patient knows who to contact and when ( Young et al, 2009 ). Therefore, Jane was advised that, should she develop chest pains, shortness of breath, peripheral oedema, reduced urinary output, headaches, visual disturbances or retinal haemorrhages ( Schroeder, 2017 ), she should present immediately to the emergency department, otherwise she would be reviewed in the surgery in 1 week.

Jane was followed up in a second consultation 1 week later with her home blood pressure readings. The average reading from the previous 6 days was calculated ( Bostock-Cox, 2013 ) and Jane's home blood pressure reading was 158/82 mmHg. This reading ruled out white-coat syndrome as Jane's blood pressure remained elevated outside clinic conditions (white-coat syndrome is defined as a difference of more than 20/10 mmHg between clinic blood pressure readings and the average home blood pressure reading; NICE, 2019 ; 2022 ). Subsequently, Jane was diagnosed with stage 2 essential (or primary) hypertension. Stage 2 is defined as a clinic blood pressure of 160/100 mmHg or higher or a home blood pressure of 150/95 mmHg or higher ( NICE, 2019 ; 2022 ).

A diagnosis of hypertension can be difficult for patients as they obtain a ‘sick label’ despite feeling well ( Jamison, 2006 ). This is recognised as a deterrent for their motivation to initiate drug treatment and lifestyle changes ( Williams, 2013 ), presenting a greater challenge to health professionals, which can be addressed through concordance strategies. However, having taken Jane's bloods, electrocardiogram and urine albumin:creatinine ratio in the first consultation, it was evident that there was no target organ damage and her Qrisk3 score was calculated as 3.4%. These results provided reassurance for Jane, but she was keen to engage and prevent any potential complications.

Agreeing treatment

Concordance is only truly practised when the patient's perspectives are valued, shared and used to inform planning ( McKinnon, 2013 ). The trainee advanced nurse practitioner now needed to use the information gained from the consultations to formulate a co-produced and meaningful treatment plan based on the best available evidence ( Diamond-Fox and Bone, 2021 ). Jane understood the risk associated with high blood pressure and was keen to begin medication as soon as possible. NICE guidelines ( 2019 ; 2022 ) advocate the use of an angiotensin-converting enzyme (ACE) inhibitor or angiotensin-receptor blockers in patients under 55 years of age and not of Black African or African-Caribbean origin. However, ACE inhibitors seem to be used as the first-line treatment for hypertensive patients under the age of 55 years ( O'Donovan, 2019 ).

ACE inhibitors directly affect the renin–angiotensin-aldosterone system which plays a central role in regulation of blood pressure ( Porth, 2015 ). Renin is secreted by the juxtaglomerular cells, in the kidneys' nephrons, when there is a decrease in renal perfusion and stimulation of the sympathetic nervous system ( O'Donovan, 2018 ). Renin then combines with angiotensinogen, a circulating plasma globulin from the liver, to form angiotensin I ( Kumar and Clark, 2017 ). Angiotensin I is inactive but, through ACE, an enzyme present in the endothelium of the lungs, it is transformed into angiotensin II ( Kumar and Clark, 2017 ). Angiotensin II is a vasoconstrictor which increases vascular resistance and in turn blood pressure ( Porth, 2015 ) while also stimulating the adrenal gland to produce aldosterone. Aldosterone reduces sodium excretion in the kidneys, thus increasing water reabsorption and therefore blood volume ( Porth, 2015 ). Using an ACE inhibitor prevents angiotensin II formation, which prevents vasoconstriction and stops reabsorption of sodium and water, thus reducing blood pressure.

When any new medication is being considered, providing education is key. This must include what the medication is for, the importance of taking it, any contraindications or interactions with the current medications being taken by the patient and the potential risk of adverse effects ( O'Donovan, 2018 ). Sharing this information with Jane allowed her to weigh up the pros and cons and make an informed choice leading to the creation of an individualised treatment plan.

Jamison (2006) placed great emphasis on sharing information about adverse effects, because patients with hypertension feel well before commencing medications, but taking medication has the potential to cause side effects which can affect adherence. Therefore, the range of side effects were discussed with Jane. These include a persistent, dry non-productive cough, hypotension, hypersensitivity, angioedema and renal impairment with hyperkalaemia ( Hitchings et al, 2019 ). ACE inhibitors have a range of adverse effects and most resolve when treatment is stopped ( Waterfield, 2008 ).

Following discussion with Jane, she proceeded with taking an ACE inhibitor and was encouraged to report any side effects in order to find another more suitable medication and to prevent her hypertension from going untreated. This information was provided verbally and written which is seen as good practice ( Green, 2015 ). Jane was followed up with fortnightly blood pressure recordings and urea and electrolyte checks and her dose of ramipril was increased fortnightly until her blood pressure was under 140/90 mmHg ( NICE, 2019 ; 2022 ).

Conclusions

Adherence to medications can be difficult to establish and maintain, especially for patients with long-term conditions. This can be particularly challenging for patients with hypertension because they are generally asymptomatic, yet acquire a sick label and start lifelong medication and lifestyle adjustments to prevent complications. Through adopting a concordant approach in practice, the outcome of adherence can be increased. This case study demonstrates how concordant strategies were implemented throughout the consultation to create a therapeutic patient–professional relationship. This optimised the creation of an individualised treatment plan which the patient engaged with and adhered to.

• Hypertension is a growing worldwide problem
• Appropriate clinical assessment, diagnosis and management is key to prevent misdiagnosis
• Long-term conditions are associated with high levels of non-adherence to treatments
• Adopting a concordance approach to practice optimises adherence and promotes positive patient outcomes

CPD reflective questions

• How has this article developed your assessment, diagnosis or management of patients presenting with a high blood pressure?
• What measures can you implement in your practice to enhance a concordant approach?

Hypertension

Learn about the nursing care management of patients with hypertension .

Table of Contents

• What is Hypertension? 

Classification

Pathophysiology, epidemiology, clinical manifestations, complications, diagnostic tests, pharmacologic therapy.

• Nursing Assessment 
• Diagnosis 
• Nursing Care Plan and Goals

Nursing Priorities

Nursing interventions, discharge and home care guidelines, documentation guidelines, what is hypertension.

Hypertension is one of the most common lifestyle diseases to date. It affects people from all walks of life. Let us get to know hypertension more by its definitions.

• Hypertension is defined as a systolic blood pressure greater than 140 mmHg and a diastolic pressure of more than 90 mmHg .
• This is based on the average of two or more accurate blood pressure measurements during two or more consultations with the healthcare provider.
• The definition is taken from the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure .

In 2017, the American College of Cardiology and the American Heart Association revised their hypertension guidelines . The previous guidelines set the threshold at 140/90 mm Hg for younger people and 150/80 mm Hg for those ages 65 and older.

• Normal . The normal range for blood pressure is between, less than 120 mmHg and less than 80 mmHg.
• Elevated . Elevated stage starts from 120 mmHg to 129 mmHg for systolic blood pressure and less than 80 mmHg for diastolic pressure.
• Stage 1 hypertension . Stage 1 starts when the patient has a systolic pressure of 130 to 139 mmHg and a diastolic pressure of 80 to 89 mmHg.
• Stage 2 hypertension . Stage 2 starts when the systolic pressure is already more than or equal than 140 mmHg and the diastolic is more than or equal than 90 mmHg.

In a normal circulation, pressure is transferred from the heart muscle to the blood each time the heart contracts and then pressure is exerted by the blood as it flows through the blood vessels.

The pathophysiology of hypertension follows.

• Hypertension is a multifactorial
• When there is excess sodium intake , renal sodium retention occurs, which increases fluid volume resulting in increased preload and increase in contractility.
• Obesity is also a factor in hypertension because hyperinsulinemia develops and structural hypertrophy results leading to increased peripheral vascular resistance.
• Genetic alteration also plays a role in the development of hypertension because when there is cell membrane alteration, functional constriction may follow and also results in increased peripheral vascular resistance.

Hypertension is slowly rising to the top as one of the primary causes of morbidity in the world . Here are the current statistics of the status of hypertension in some of the leading countries.

• About 31% of the adults in the United States have hypertension.
• African-Americans have the highest prevalence rate of 37%.
• In the total US population of persons with hypertension, 90% to 95% have primary hypertension or high blood pressure from an unidentified cause.
• The remaining 5% to 10% of this group have secondary hypertension or high blood pressure related to identified causes.
• Hypertension is also termed as the “silent killer” because 24% of people who had pressures exceeding 140/90 mmHg were unaware that their blood pressures were elevated.

Hypertension has a lot of causes just like how  fever has many causes. The factors that are implicated as causes of hypertension are:

• Increased sympathetic nervous system activity . Sympathetic nervous system activity increases because there is dysfunction in the autonomic nervous system .
• Increase renal reabsorption . There is an increase reabsorption of sodium, chloride, and water which is related to a genetic variation in the pathways by which the kidneys handle sodium.
• Increased RAAS activity . The renin-angiotensin-aldosterone system increases its activity leading to the expansion of extracellular fluid volume and increased systemic vascular resistance.
• Decreased vasodilation of the arterioles . The vascular endothelium is damaged because of the decrease in the vasodilation of the arterioles.

Many people who have hypertension are asymptomatic at first. Physical examination may reveal no abnormalities except for an elevated blood pressure, so one must be prepared to recognize hypertension at its earliest.

• Headache . The red blood cells carrying oxygen is having a hard time reaching the brain because of constricted vessels , causing headache.
• Dizziness occurs due to the low concentration of oxygen that reaches the brain.
• Chest pain . Chest pain occurs also due to decreased oxygen levels .
• Blurred vision. Blurred vision may occur later on because of too much constriction in the blood vessels of the eye that red blood cells carrying oxygen cannot pass through.

Prevention of hypertension mainly relies on a healthy lifestyle and self-discipline.

• Weight reduction . Maintenance of normal body weight can help prevent hypertension.
• Adopt DASH . DASH or the Dietary Approaches to Stop Hypertension includes consummation of a diet rich in fruits, vegetable, and low-fat dairy .
• Dietary sodium retention . Sodium contributes to an elevated blood pressure, so reducing the dietary intake to no more than 2.4 g sodium per day can be really helpful.
• Physical activity . Engage in regular aerobic physical activity for 30 minutes thrice every week.
• Moderation of alcohol consumption . Limit alcohol consumption to no more than 2 drinks per day in men and one drink for women and people who are lighter in weight.

If hypertension is left untreated, it could progress to complications of the different body organs.

• Heart failure . With increased blood pressure, the heart pumps blood faster than normal until the heart muscle goes weak from too much exertion.
• Myocardial infarction . Decreased oxygen due to constriction of blood vessels may lead to MI.
• Impaired vision. Ineffective peripheral perfusion affects the eye, causing problems in vision because of decreased oxygen.
• Renal failure. Blood carrying oxygen and nutrients could not reach the renal system because of the constricted blood vessels .

Assessment and Diagnostic Findings

Assessment of the patient with hypertension must be detailed and thorough. There are also diagnostic tests that can be performed to establish the diagnosis of hypertension.

• Assess the patient’s health history
• Perform physical examination as appropriate.
• The retinas are examined to assess possible organ damage .
• Laboratory tests are also taken to check target organ damage .
• Urinalysis is performed to check the concentration of sodium in the urine though the specific gravity.
• Blood chemistry (e.g. analysis of sodium, potassium , creatinine , fasting glucose , and total and high density lipoprotein cholesterol levels). These tests are done to determine the level of sodium and fat in the body.
• 12-lead ECG . ECG needs to be performed to rule presence of cardiovascular damage .
• Echocardiography . Echocardiography assesses the presence of left ventricular hypertrophy .
• Creatinine clearance . Creatinine clearance is performed to check for the level of BUN and creatinine that can determine if there is renal damage or not.
• Renin level . Renin level should be assessed to determine how RAAS is coping.
• Hemoglobin/hematocrit:  Not diagnostic but assesses relationship of cells to fluid volume (viscosity) and may indicate risk factors such as hypercoagulability, anemia .
• Blood urea nitrogen (BUN)/creatinine:  Provides information about renal perfusion/function.
• Glucose:  Hyperglycemia ( diabetes mellitus is a precipitator of hypertension) may result from elevated catecholamine levels (increases hypertension).
• Serum potassium :   Hypokalemia may indicate the presence of primary aldosteronism (cause) or be a side effect of diuretic ­therapy.
• Serum calcium :  Imbalance may contribute to hypertension.
• Lipid panel (total lipids, high-density lipoprotein [HDL], low-density lipoprotein [LDL], cholesterol, triglycerides, phospholipids):  Elevated level may indicate predisposition for/presence of atheromatous plaques.
• Thyroid studies:  Hyperthyroidism may lead or contribute to vasoconstriction and hypertension.
• Serum/urine aldosterone level:  May be done to assess for primary aldosteronism (cause).
• Urinalysis:  May show blood, protein, or white blood cells; or glucose suggests renal dysfunction and/or presence of diabetes .
• Creatinine clearance:  May be reduced, reflecting renal damage.
• Urine vanillylmandelic acid (VMA) (catecholamine metabolite):  Elevation may indicate presence of pheochromocytoma (cause); 24-hour urine VMA may be done for assessment of pheochromocytoma if hypertension is intermittent.
• Uric acid:  Hyperuricemia has been implicated as a risk factor for the development of hypertension.
• Renin:  Elevated in renovascular and malignant hypertension, salt-wasting disorders.
• Urine steroids:  Elevation may indicate hyperadrenalism, pheochromocytoma, pituitary dysfunction, Cushing’s syndrome.
• Intravenous pyelogram (IVP):  May identify cause of secondary hypertension, e.g., renal parenchymal disease, renal/ureteral ­calculi.
• Kidney and renography nuclear scan:  Evaluates renal status (TOD).
• Excretory urography:  May reveal renal atrophy, indicating chronic renal disease.
• Chest x-ray :  May demonstrate obstructing calcification in valve areas; deposits in and/or notching of aorta ; cardiac enlargement.
• Computed tomography (CT) scan:  Assesses for cerebral tumor , CVA, or encephalopathy or to rule out pheochromocytoma.
• Electrocardiogram (ECG):  May demonstrate enlarged heart, strain patterns, conduction disturbances. Note: Broad, notched P wave is one of the earliest signs of hypertensive heart disease.

Medical Management

Main Topic: Antihypertensive Drugs

The goal of hypertensive treatment I to prevent complications and death by achieving and maintaining the arterial blood pressure at 40/90 mmHg or lower.

• The medications used for treating hypertension decrease peripheral resistance , blood volume , or the strength and rate of myocardial contraction .
• For uncomplicated hypertension, the initial medications recommended are diuretics and beta blockers.
• Only low doses are given, but if blood pressure still exceeds 140/90 mmHg, the dose is increased gradually.
• Thiazide diuretics decrease blood volume , renal blood flow, and cardiac output.
• ARBs are competitive inhibitors of aldosterone binding .
• Beta blockers block the sympathetic nervous system to produce a slower heart rate and a lower blood pressure.
• ACE inhibitors inhibit the conversion of angiotensin I to angiotensin II and lowers peripheral resistance.

Stage 1 Hypertension

• Thiazide diuretic is recommended for most and angiotensin-converting enzyme-1, aldosterone receptor blocker , beta blocker , or calcium channel blocker is considered.

Stage 2 Hypertension

• Two-drug combination is followed, usually including thiazide diuretic and angiotensin-converting enzyme-1, or beta-blocker , or calcium channel blocker.

Nursing Management

The goal of nursing management is to help achieve a normal blood pressure through independent and dependent interventions.

Nursing Assessment

Nursing assessment must involve careful monitoring of the blood pressure at frequent and routinely scheduled intervals.

• If patient is on antihypertensive medications, blood pressure is assessed to determine the effectiveness and detect changes in the blood pressure.
• Complete history should be obtained to assess for signs and symptoms that indicate target organ damage.
• Pay attention to the rate, rhythm, and character of the apical and peripheral pulses.

Based on the assessment data, nursing diagnoses may include the following:

• Deficient knowledge regarding the relation between the treatment regimen and control of the disease process.
• Noncompliance with the therapeutic regimen related to side effects of the prescribed therapy.
• Risk for activity intolerance related to imbalance between oxygen supply and demand.
• Risk- prone health behavior related to condition requiring change in lifestyle.

Nursing Care Plan and Goals

Main article: 6 Hypertension Nursing Care Plans

The major goals for a patient with hypertension are as follows:

• Understanding of the disease process and its treatment.
• Participation in a self-care program.
• Absence of complications.
• BP within acceptable limits for individual.
• Cardiovascular and systemic complications prevented/minimized.
• Disease process/prognosis and therapeutic regimen understood.
• Necessary lifestyle/behavioral changes initiated.
• Plan in place to meet needs after discharge.
• Maintain/enhance cardiovascular functioning.
• Prevent complications.
• Provide information about disease process/prognosis and treatment regimen.
• Support active patient control of condition.

The objective of nursing care focuses on lowering and controlling the blood pressure without adverse effects and without undue cost.

• Encourage the patient to consult a dietitian to help develop a plan for improving nutrient intake or for weight loss .
• Encourage restriction of sodium and fat
• Emphasize increase intake of fruits and vegetables .
• Implement regular physical activity .
• Advise patient to limit alcohol consumption and avoidance of tobacco.
• Assist the patient to develop and adhere to an appropriate exercise regimen.  

At the end of the treatment regimen, the following are expected to be achieved:

• Maintain blood pressure at less than 140/90 mmHg with lifestyle modifications, medications, or both.
• Demonstrate no symptoms of angina , palpitations, or visual changes.
• Has stable BUN and serum creatinine levels.
• Has palpable peripheral pulses.
• Adheres to the dietary regimen as prescribed.
• Exercises regularly.
• Takes medications as prescribed and reports side effects.
• Measures blood pressure routinely.
• Abstains from tobacco and alcohol intake.
• Exhibits no complications.

Following discharge, the nurse should promote self-care and independence of the patient.

• The nurse can help the patient achieve blood pressure control through education about managing blood pressure.
• Assist the patient in setting goal blood pressures .
• Provide assistance with social support.
• Encourage the involvement of family members in the education program to support the patient’s efforts to control hypertension.
• Provide written information about expected effects and side effects.
• Encourage and teach patients to measure their blood pressures at home.
• Emphasize strict compliance of follow-up check up .

These are the following data that should be documented for the patient’s record:

• Effects of behavior on health status/condition.
• Plan for adjustments and interventions for achieving the plan and the people involved.
• Client responses to the interventions, teaching, and action plan performed.
• Attainment or progress towards desired outcome.
• Modifications to plan care.
• Individual findings including deviation from prescribed treatment plan.
• Consequences of actions to date.

Posts related to Hypertension:

• Pregnancy Induced Hypertension
• 6 Hypertension Nursing Care Plans
• Antihypertensive Drugs
• Cardiovascular Care Nursing Mnemonics and Tips

5 thoughts on “Hypertension”

I want some NMC questions to solve

Question regarding Stage 1 HTN is incorrect. Stage 1 HTN is BP reading 140-159/90-99.

In new version of Brunner & Suddath’s medical surgical nursing textbook (2022), stage 1 HTN is BP reading 130-139/80-89. (pp: 866, vol 1)

I don’t understand the explanation for the classification of hypertension, the explanation is not matching with the table, why?

“Medical Management Main Topic: Antihypertensive Drugs

The goal of hypertensive treatment I to prevent complications and death by achieving and maintaining the arterial blood pressure at 40/90 mmHg or lower.”

I think need to correct the above sentence as follows;

The goal of hypertensive treatment is to prevent complications and death by achieving and maintaining the arterial blood pressure at 140/90 mmHg or lower.”

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Next Generation NCLEX Case Study Sample Questions

One of the big changes on the Next Generation NCLEX exam is a shift toward case studies. Case studies often require a deeper level of critical thinking, and understanding diseases on a more in-depth level (especially the pathophysiology) will make these types of questions easier to answer.

In this article, you’ll be able to watch a free video to help you prepare for the new Next Generation NCLEX case study format. Nurse Sarah will walk you step-by-step through each scenario and help you understand how to use critical thinking and nursing knowledge to answer these types of questions.

Next Generation NCLEX Case Study Review Questions Video

NGN Case Study Sample Questions and Answers

First, let’s take a look at our case study summary below:

Case Study Summary:

A 68-year-old male is admitted with shortness of breath. He reports difficulty breathing with activity, lying down, or while sleeping. He states that in order to “breathe easier,” he has had to sleep in a recliner for the past week. The patient has a history of hypertension, myocardial infarction (2 years ago), and cholecystectomy (10 years ago). The patient is being transferred to a cardiac progressive care unit for further evaluation and treatment.

Question 1 of 6: The nurse receives the patient admitted with shortness of breath. What findings are significant and require follow-up? The options are listed below. Select all that apply.

To answer this first question in the NGN case study, let’s look at the information provided in the nursing notes and vital signs tabs provided:

This question is asking us to identify findings that are significant and require the nurse to follow-up. In other words, what is presenting that we can’t ignore but need to investigate further.

Therefore, let’s comb through the nursing notes and vital signs to see what is abnormal and requires follow-up.

First, the patient arrived to the room via stretcher. That’s fine and doesn’t necessarily require follow-up.

Next, the patient is alert and oriented x 4 (person, place, time, event). This tells us that the patient’s neuro status is intact so far. Therefore, the shortness of breath isn’t affecting the patient’s mental function yet (we have enough oxygen on board right now for brain activity).

However, the nurse has noticed the shortness of breath with activity and talking, which should not normally happen. This tells us something is wrong and is significant enough to require follow-up. We want to know why is this happening, is it going to get worse, etc.

The patient’s weight and vital signs were collected (this is good). Weight is 155 lbs. and BMI is within a healthy range (doesn’t tell us too much but may be useful later). The patient is also connected to a bedside monitor, so they need to be monitored constantly like on a progressive care unit.

The monitor shows sinus tachycardia . This is significant because it seems the patient’s shortness of breath is causing the heart to compensate by increasing the heart rate to provide more oxygen (hence the lungs may be compromised).

Then we find out that the lungs are indeed compromised because crackles are heard in both lungs , and this may be why our patient is short of breath. This is significant (could the patient have pulmonary edema?)

Then we find out the nurse has noted an S3. This is an extra heart sound noted after S2. And what jumps out to me about this is that it is usually associated with volume overload in the heart like in cases of heart failure . However, S3 may be normal in some people under 40 or during pregnancy, but that’s not the case with our patient based on what we read in the case summary.

Therefore, based on everything I’m reading in this case study, I’m thinking this patient may have heart failure, but we need those test results back (especially the echo and chest x-ray, and hopefully a BNP will be in there too).

We are also told that the patient has an 18 gauge IV inserted (which is good thing to have so we can give medications if required), orders have been received, labs drawn, and testing results are pending.

Now let’s look at the “Vital Signs” tab above, and ask yourself what is normal vs. abnormal for this patient (adult male).

• The heart rate is high at 112 (tachycardia), and should normally be 60-100 bpm (see heart rhythms ).
• Blood pressure is higher than normal (normal is 120/80), which indicates hypertension.
• Oxygen saturation is 94% (this is on the low side as we’d normally want around 95% or higher, and the patient is on 4 L nasal cannula, which tells us the lungs are not okay).
• Respiratory rate is increased (26 breaths per minute)…normal is 12-20 breaths per minute.

Based on the information we were provided, I’ve selected the answers below. These findings are significant and definitely require follow-up by the nurse.

When answering these NGN case study questions, it’s helpful to think of the ABCDE (airway, breathing, circulation, etc.) as all of these fall into that category. If we don’t follow-up on the shortness of breath, crackles, respiratory rate, o2 saturation (94% on 4 L nasal cannula), the respiratory system can further decline.

In addition, the sinus tachycardia, S3 gallop, and hypertension could indicate fluid overload in the heart. This may cause the heart to tire out and lead the lethal rhythm. On the other hand, temperature, pain, weight, and BMI are not abnormal and do not require follow-up.

See the Complete Next Generation NCLEX Case Study Review

Each question in the case study builds on the previous question. To see how these questions evolve based on the patient’s condition and labs, watch the entire Next Generation NCLEX Case Study Review video on our YouTube Channel (RegisteredNurseRN).

NCLEX Practice Quizzes

We’ve developed many free NCLEX review quizzes to test your knowledge on nursing topics and to help you prepare for the Next Generation NCLEX exam.

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Patient Case Presentation

Mr. E.A. is a 40-year-old black male who presented to his Primary Care Provider for a diabetes follow up on October 14th, 2019. The patient complains of a general constant headache that has lasted the past week, with no relieving factors. He also reports an unusual increase in fatigue and general muscle ache without any change in his daily routine. Patient also reports occasional numbness and tingling of face and arms. He is concerned that these symptoms could potentially be a result of his new diabetes medication that he began roughly a week ago. Patient states that he has not had any caffeine or smoked tobacco in the last thirty minutes. During assessment vital signs read BP 165/87, Temp 97.5 , RR 16, O 98%, and HR 86. E.A states he has not lost or gained any weight. After 10 mins, the vital signs were retaken BP 170/90, Temp 97.8, RR 15, O 99% and HR 82. Hg A1c 7.8%, three months prior Hg A1c was 8.0%.  Glucose  180 mg/dL (fasting).  FAST test done; negative for stroke. CT test, Chem 7 and CBC have been ordered.

Past medical history

Diagnosed with diabetes (type 2) at 32 years old

Overweight, BMI of 31

Had a cholecystomy at 38 years old

Diagnosed with dyslipidemia at 32 years old

Past family history

Mother alive, diagnosed diabetic at 42 years old 

Father alive with Hypertension diagnosed at 55 years old

Brother alive and well at 45 years old

Sister alive and obese at 34 years old 

Pertinent social history

Social drinker on occasion

Smokes a pack of cigarettes per day

Works full time as an IT technician and is in graduate school

PICO: Form a Focused Clinical Question

• 1. Ask: PICO(T) Question
• 2. Align: Levels of Evidence
• 3a. Acquire: Resource Types
• 3b. Acquire: Searching
• 4. Appraise
• Primary vs. Secondary Sources
• Case Study Example
• Practice PICO

Formulate a Clinical Question from a Case Study

• Case: Hypertension

I: Intervention

C: comparison.

• PICO: Putting It Together

Clinical Scenario

A 68-year-old female patient has recently been diagnosed with high blood pressure. She is otherwise healthy and active. You need to decide whether to prescribe her a beta-blocker or an ACE inhibiter.

Image:  "Blood pressure measuring. Doctor and patient. Health care."  by  agilemktg1  is marked with  CC PDM 1.0

► Click on the P: Patient tab to proceed in developing a clinical question.

(Case study from EBM Librarian: Teaching Tools: Scenarios .)

Consider when choosing your patient/problem:

• What are the most important characteristics?
• Relevant demographic factors
• The setting

Patient: adult hypertensive female

Image: "Nurse measuring blood pressure of senior woman at home. Looking at camera, smiling.?"  by  agilemktg1  is marked with  CC PDM 1.0

► Click on the I: Intervention tab to proceed in developing a clinical question.

Consider for your intervention:

• What is the main intervention, treatment, diagnostic test, procedure, or exposure?
• Think of dosage, frequency, duration, and mode of delivery

Intervention: beta-blocker

Image:  "Atenolol Blood Pressure Tablets Image 4"  by  Doctor4U_UK  is licensed under  CC BY 2.0

► Click on the C: Comparison tab to proceed in developing a clinical question.

Consider for your comparison:

• Inactive control intervention: Placebo, standard care, no treatment
• Active control intervention: A different drug, dose, or kind of therapy

Comparison: ACE   inhibiter

Image:  "Ramipril Blood Pressure Capsules Image 5"  by  Doctor4U_UK  is licensed under  CC BY 2.0

► Click on the O: Outcome  tab to proceed in developing a clinical question.

Consider for your outcome:

• Be specific and make it measurable
• It can be something objective or subjective

Outcome: relief of symptoms; controlled blood pressure

Image:  "File:BP B6 Connect blood pressure monitor.png"  by  百略醫學  is licensed under  CC BY-SA 4.0

► Click on the PICO: Putting It Together  tab to proceed in developing a clinical question.

Formulate a PICO Question

Answerable PICO Question: In middle-aged adult females with hypertension, are beta blockers more effective than ACE inhibiters in controlling blood pressure?

Image:  "Dagstuhl 2008-02-01 - 37"  by  Nic's events  is licensed under  CC BY-SA 2.0

Suggested MeSH Terms:  Adrenergic beta-Antagonists/therapeutic use; Angiotensin-Converting Enzyme Inhibitors/therapeutic use; hypertension/drug therapy

Tip: Incorporating sex into the search may not be necessary unless there is a significant difference between males and females in relevant studies. 

Click "Next" below to practice formulating clinical questions using PICO format.

• << Previous: Primary vs. Secondary Sources
• Next: Practice PICO >>
• Last Updated: Oct 5, 2023 2:35 PM
• URL: https://med-fsu.libguides.com/pico

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Article Contents

Clinical management and treatment decisions, hypertension in black americans, pharmacologic treatment of hypertension in black americans.

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Suzanne Oparil, Case study, American Journal of Hypertension , Volume 11, Issue S8, November 1998, Pages 192S–194S, https://doi.org/10.1016/S0895-7061(98)00195-2

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Ms. C is a 42-year-old black American woman with a 7-year history of hypertension first diagnosed during her last pregnancy. Her family history is positive for hypertension, with her mother dying at 56 years of age from hypertension-related cardiovascular disease (CVD). In addition, both her maternal and paternal grandparents had CVD.

At physician visit one, Ms. C presented with complaints of headache and general weakness. She reported that she has been taking many medications for her hypertension in the past, but stopped taking them because of the side effects. She could not recall the names of the medications. Currently she is taking 100 mg/day atenolol and 12.5 mg/day hydrochlorothiazide (HCTZ), which she admits to taking irregularly because “... they bother me, and I forget to renew my prescription.” Despite this antihypertensive regimen, her blood pressure remains elevated, ranging from 150 to 155/110 to 114 mm Hg. In addition, Ms. C admits that she has found it difficult to exercise, stop smoking, and change her eating habits. Findings from a complete history and physical assessment are unremarkable except for the presence of moderate obesity (5 ft 6 in., 150 lbs), minimal retinopathy, and a 25-year history of smoking approximately one pack of cigarettes per day. Initial laboratory data revealed serum sodium 138 mEq/L (135 to 147 mEq/L); potassium 3.4 mEq/L (3.5 to 5 mEq/L); blood urea nitrogen (BUN) 19 mg/dL (10 to 20 mg/dL); creatinine 0.9 mg/dL (0.35 to 0.93 mg/dL); calcium 9.8 mg/dL (8.8 to 10 mg/dL); total cholesterol 268 mg/dL (< 245 mg/dL); triglycerides 230 mg/dL (< 160 mg/dL); and fasting glucose 105 mg/dL (70 to 110 mg/dL). The patient refused a 24-h urine test.

Taking into account the past history of compliance irregularities and the need to take immediate action to lower this patient’s blood pressure, Ms. C’s pharmacologic regimen was changed to a trial of the angiotensin-converting enzyme (ACE) inhibitor enalapril, 5 mg/day; her HCTZ was discontinued. In addition, recommendations for smoking cessation, weight reduction, and diet modification were reviewed as recommended by the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI). 1

After a 3-month trial of this treatment plan with escalation of the enalapril dose to 20 mg/day, the patient’s blood pressure remained uncontrolled. The patient’s medical status was reviewed, without notation of significant changes, and her antihypertensive therapy was modified. The ACE inhibitor was discontinued, and the patient was started on the angiotensin-II receptor blocker (ARB) losartan, 50 mg/day.

After 2 months of therapy with the ARB the patient experienced a modest, yet encouraging, reduction in blood pressure (140/100 mm Hg). Serum electrolyte laboratory values were within normal limits, and the physical assessment remained unchanged. The treatment plan was to continue the ARB and reevaluate the patient in 1 month. At that time, if blood pressure control remained marginal, low-dose HCTZ (12.5 mg/day) was to be added to the regimen.

Hypertension remains a significant health problem in the United States (US) despite recent advances in antihypertensive therapy. The role of hypertension as a risk factor for cardiovascular morbidity and mortality is well established. 2–7 The age-adjusted prevalence of hypertension in non-Hispanic black Americans is approximately 40% higher than in non-Hispanic whites. 8 Black Americans have an earlier onset of hypertension and greater incidence of stage 3 hypertension than whites, thereby raising the risk for hypertension-related target organ damage. 1 , 8 For example, hypertensive black Americans have a 320% greater incidence of hypertension-related end-stage renal disease (ESRD), 80% higher stroke mortality rate, and 50% higher CVD mortality rate, compared with that of the general population. 1 , 9 In addition, aging is associated with increases in the prevalence and severity of hypertension. 8

Research findings suggest that risk factors for coronary heart disease (CHD) and stroke, particularly the role of blood pressure, may be different for black American and white individuals. 10–12 Some studies indicate that effective treatment of hypertension in black Americans results in a decrease in the incidence of CVD to a level that is similar to that of nonblack American hypertensives. 13 , 14

Data also reveal differences between black American and white individuals in responsiveness to antihypertensive therapy. For instance, studies have shown that diuretics 15 , 16 and the calcium channel blocker diltiazem 16 , 17 are effective in lowering blood pressure in black American patients, whereas β-adrenergic receptor blockers and ACE inhibitors appear less effective. 15 , 16 In addition, recent studies indicate that ARB may also be effective in this patient population.

Angiotensin-II receptor blockers are a relatively new class of agents that are approved for the treatment of hypertension. Currently, four ARB have been approved by the US Food and Drug Administration (FDA): eprosartan, irbesartan, losartan, and valsartan. Recently, a 528-patient, 26-week study compared the efficacy of eprosartan (200 to 300 mg/twice daily) versus enalapril (5 to 20 mg/daily) in patients with essential hypertension (baseline sitting diastolic blood pressure [DBP] 95 to 114 mm Hg). After 3 to 5 weeks of placebo, patients were randomized to receive either eprosartan or enalapril. After 12 weeks of therapy within the titration phase, patients were supplemented with HCTZ as needed. In a prospectively defined subset analysis, black American patients in the eprosartan group (n = 21) achieved comparable reductions in DBP (−13.3 mm Hg with eprosartan; −12.4 mm Hg with enalapril) and greater reductions in systolic blood pressure (SBP) (−23.1 with eprosartan; −13.2 with enalapril), compared with black American patients in the enalapril group (n = 19) ( Fig. 1 ). 18 Additional trials enrolling more patients are clearly necessary, but this early experience with an ARB in black American patients is encouraging.

Efficacy of the angiotensin II receptor blocker eprosartan in black American with mild to moderate hypertension (baseline sitting DBP 95 to 114 mm Hg) in a 26-week study. Eprosartan, 200 to 300 mg twice daily (n = 21, solid bar), enalapril 5 to 20 mg daily (n = 19, diagonal bar). †10 of 21 eprosartan patients and seven of 19 enalapril patients also received HCTZ. Adapted from data in Levine: Subgroup analysis of black hypertensive patients treated with eprosartan or enalapril: results of a 26-week study, in Programs and abstracts from the 1st International Symposium on Angiotensin-II Antagonism, September 28–October 1, 1997, London, UK.

Approximately 30% of all deaths in hypertensive black American men and 20% of all deaths in hypertensive black American women are attributable to high blood pressure. Black Americans develop high blood pressure at an earlier age, and hypertension is more severe in every decade of life, compared with whites. As a result, black Americans have a 1.3 times greater rate of nonfatal stroke, a 1.8 times greater rate of fatal stroke, a 1.5 times greater rate of heart disease deaths, and a 5 times greater rate of ESRD when compared with whites. 19 Therefore, there is a need for aggressive antihypertensive treatment in this group. Newer, better tolerated antihypertensive drugs, which have the advantages of fewer adverse effects combined with greater antihypertensive efficacy, may be of great benefit to this patient population.

1. Joint National Committee : The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure . Arch Intern Med 1997 ; 24 157 : 2413 – 2446 .

Google Scholar

2. Veterans Administration Cooperative Study Group on Antihypertensive Agents : Effects of treatment on morbidity in hypertension: Results in patients with diastolic blood pressures averaging 115 through 129 mm Hg . JAMA 1967 ; 202 : 116 – 122 .

3. Veterans Administration Cooperative Study Group on Antihypertensive Agents : Effects of treatment on morbidity in hypertension: II. Results in patients with diastolic blood pressures averaging 90 through 114 mm Hg . JAMA 1970 ; 213 : 1143 – 1152 .

4. Pooling Project Research Group : Relationship of blood pressure, serum cholesterol, smoking habit, relative weight and ECG abnormalities to the incidence of major coronary events: Final report of the pooling project . J Chronic Dis 1978 ; 31 : 201 – 306 .

5. Hypertension Detection and Follow-Up Program Cooperative Group : Five-year findings of the hypertension detection and follow-up program: I. Reduction in mortality of persons with high blood pressure, including mild hypertension . JAMA 1979 ; 242 : 2562 – 2577 .

6. Kannel WB , Dawber TR , McGee DL : Perspectives on systolic hypertension: The Framingham Study . Circulation 1980 ; 61 : 1179 – 1182 .

7. Hypertension Detection and Follow-Up Program Cooperative Group : The effect of treatment on mortality in “mild” hypertension: Results of the Hypertension Detection and Follow-Up Program . N Engl J Med 1982 ; 307 : 976 – 980 .

8. Burt VL , Whelton P , Roccella EJ et al.  : Prevalence of hypertension in the US adult population: Results from the third National Health and Nutrition Examination Survey, 1988–1991 . Hypertension 1995 ; 25 : 305 – 313 .

9. Klag MJ , Whelton PK , Randall BL et al.  : End-stage renal disease in African-American and white men: 16-year MRFIT findings . JAMA 1997 ; 277 : 1293 – 1298 .

10. Neaton JD , Kuller LH , Wentworth D et al.  : Total and cardiovascular mortality in relation to cigarette smoking, serum cholesterol concentration, and diastolic blood pressure among black and white males followed up for five years . Am Heart J 1984 ; 3 : 759 – 769 .

11. Gillum RF , Grant CT : Coronary heart disease in black populations II: Risk factors . Heart J 1982 ; 104 : 852 – 864 .

12. M’Buyamba-Kabangu JR , Amery A , Lijnen P : Differences between black and white persons in blood pressure and related biological variables . J Hum Hypertens 1994 ; 8 : 163 – 170 .

13. Hypertension Detection and Follow-up Program Cooperative Group : Five-year findings of the Hypertension Detection and Follow-up Program: mortality by race-sex and blood pressure level: a further analysis . J Community Health 1984 ; 9 : 314 – 327 .

14. Ooi WL , Budner NS , Cohen H et al.  : Impact of race on treatment response and cardiovascular disease among hypertensives . Hypertension 1989 ; 14 : 227 – 234 .

15. Weinberger MH : Racial differences in antihypertensive therapy: evidence and implications . Cardiovasc Drugs Ther 1990 ; 4 ( suppl 2 ): 379 – 392 .

16. Materson BJ , Reda DJ , Cushman WC et al.  : Single-drug therapy for hypertension in men: A comparison of six antihypertensive agents with placebo . N Engl J Med 1993 ; 328 : 914 – 921 .

17. Materson BJ , Reda DJ , Cushman WC for the Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents : Department of Veterans Affairs single-drug therapy of hypertension study: Revised figures and new data . Am J Hypertens 1995 ; 8 : 189 – 192 .

18. Levine B : Subgroup analysis of black hypertensive patients treated with eprosartan or enalapril: results of a 26-week study , in Programs and abstracts from the first International Symposium on Angiotensin-II Antagonism , September 28 – October 1 , 1997 , London, UK .

19. American Heart Association: 1997 Heart and Stroke Statistical Update . American Heart Association , Dallas , 1997 .

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Nursing case management for people with hypertension: A randomized controlled trial protocol

Affiliation.

• 1 Department of Urology, People's Hospital of Chengyang District, Qingdao, China.
• PMID: 33350776
• PMCID: PMC7769350
• DOI: 10.1097/MD.0000000000023850

Objective: To explore the effect of management of nursing case on blood pressure control in hypertension patients.

Method: This is a randomized controlled study which will be carried out from May 2021 to May 2022. The experiment was granted through the Research Ethics Committee of the People's Hospital of Chengyang District (03982808). Our research includes 200 patients. Patients who meet the following conditions will be included in this experiment: the patients aged 18 to 60 years; the patients had the diagnosis of hypertension; and the urban residents. While patients with the following conditions will be excluded: having renal failure, liver failure, heart and respiratory failure; and known pregnancy. Primary result is blood pressure, while secondary results are treatment compliance, waist circumference, body mass index (BMI), type and number of antihypertensive agents used, and the existence of metabolic and cardiovascular comorbidities.

Results: Table 1 shows the clinical outcomes between the two groups.

Conclusion: Nursing case management is effective to improve the prognosis of hypertension patients.

Copyright © 2020 the Author(s). Published by Wolters Kluwer Health, Inc.

Publication types

• Clinical Trial Protocol
• Case Management / organization & administration*
• Hypertension* / diagnosis
• Hypertension* / nursing
• Nursing Care / methods*
• Outcome and Process Assessment, Health Care
• Practice Patterns, Nurses'
• Randomized Controlled Trials as Topic

Grants and funding

• 2013-WSZD120/Qingdao Health Bureau project

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A 21-Year-Old Pregnant Woman with Hypertension and Proteinuria

• Andrea Luk,

* To whom correspondence should be addressed. E-mail: [email protected]

• Ching Wan Lam,
• Wing Hung Tam,
• Anthony W. I Lo,
• Enders K. W Ng,
• Alice P. S Kong,
• Wing Yee So,
• Chun Chung Chow
• Andrea Luk, 
• Ronald C. W Ma, 
• Ching Wan Lam, 
• Wing Hung Tam, 
• Anthony W. I Lo, 
• Enders K. W Ng, 
• Alice P. S Kong, 
• Wing Yee So, 

Published: February 24, 2009

• https://doi.org/10.1371/journal.pmed.1000037
• Reader Comments

Citation: Luk A, Ma RCW, Lam CW, Tam WH, Lo AWI, Ng EKW, et al. (2009) A 21-Year-Old Pregnant Woman with Hypertension and Proteinuria. PLoS Med 6(2): e1000037. https://doi.org/10.1371/journal.pmed.1000037

Copyright: © 2009 Luk et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: The authors received no specific funding for this article.

Competing interests: RCWM is Section Editor of the Learning Forum. The remaining authors have declared that no competing interests exist.

Abbreviations: CT, computer tomography; I, iodine; MIBG, metaiodobenzylguanidine; MRI, magnetic resonance imaging; SDH, succinate dehydrogenase; SDHD, succinate dehydrogenase subunit D

Provenance: Commissioned; externally peer reviewed

Description of Case

A 21-year-old pregnant woman, gravida 2 para 1, presented with hypertension and proteinuria at 20 weeks of gestation. She had a history of pre-eclampsia in her first pregnancy one year ago. During that pregnancy, at 39 weeks of gestation, she developed high blood pressure, proteinuria, and deranged liver function. She eventually delivered by emergency caesarean section following failed induction of labour. Blood pressure returned to normal post-partum and she received no further medical follow-up. Family history was remarkable for her mother's diagnosis of hypertension in her fourth decade. Her father and five siblings, including a twin sister, were healthy. She did not smoke nor drink any alcohol. She was not taking any regular medications, health products, or herbs.

At 20 weeks of gestation, blood pressure was found to be elevated at 145/100 mmHg during a routine antenatal clinic visit. Aside from a mild headache, she reported no other symptoms. On physical examination, she was tachycardic with heart rate 100 beats per minute. Body mass index was 16.9 kg/m 2 and she had no cushingoid features. Heart sounds were normal, and there were no signs suggestive of congestive heart failure. Radial-femoral pulses were congruent, and there were no audible renal bruits.

Baseline laboratory investigations showed normal renal and liver function with normal serum urate concentration. Random glucose was 3.8 mmol/l. Complete blood count revealed microcytic anaemia with haemoglobin level 8.3 g/dl (normal range 11.5–14.3 g/dl) and a slightly raised platelet count of 446 × 10 9 /l (normal range 140–380 × 10 9 /l). Iron-deficient state was subsequently confirmed. Quantitation of urine protein indicated mild proteinuria with protein:creatinine ratio of 40.6 mg/mmol (normal range <30 mg/mmol in pregnancy).

What Were Our Differential Diagnoses?

An important cause of hypertension that occurs during pregnancy is pre-eclampsia. It is a condition unique to the gravid state and is characterised by the onset of raised blood pressure and proteinuria in late pregnancy, at or after 20 weeks of gestation [ 1 ]. Pre-eclampsia may be associated with hyperuricaemia, deranged liver function, and signs of neurologic irritability such as headaches, hyper-reflexia, and seizures. In our patient, hypertension developed at a relatively early stage of pregnancy than is customarily observed in pre-eclampsia. Although she had proteinuria, it should be remembered that this could also reflect underlying renal damage due to chronic untreated hypertension. Additionally, her electrocardiogram showed left ventricular hypertrophy, which was another indicator of chronicity.

While pre-eclampsia might still be a potential cause of hypertension in our case, the possibility of pre-existing hypertension needed to be considered. Box 1 shows the differential diagnoses of chronic hypertension, including essential hypertension, primary hyperaldosteronism related to Conn's adenoma or bilateral adrenal hyperplasia, Cushing's syndrome, phaeochromocytoma, renal artery stenosis, glomerulopathy, and coarctation of the aorta.

Box 1: Causes of Hypertension in Pregnancy

• Pre-eclampsia
• Essential hypertension
• Renal artery stenosis
• Glomerulopathy
• Renal parenchyma disease
• Primary hyperaldosteronism (Conn's adenoma or bilateral adrenal hyperplasia)
• Cushing's syndrome
• Phaeochromocytoma
• Coarctation of aorta
• Obstructive sleep apnoea

Renal causes of hypertension were excluded based on normal serum creatinine and a bland urinalysis. Serology for anti-nuclear antibodies was negative. Doppler ultrasonography of renal arteries showed normal flow and no evidence of stenosis. Cushing's syndrome was unlikely as she had no clinical features indicative of hypercortisolism, such as moon face, buffalo hump, violaceous striae, thin skin, proximal muscle weakness, or hyperglycaemia. Plasma potassium concentration was normal, although normokalaemia does not rule out primary hyperaldosteronism. Progesterone has anti-mineralocorticoid effects, and increased placental production of progesterone may mask hypokalaemia. Besides, measurements of renin activity and aldosterone concentration are difficult to interpret as the renin-angiotensin-aldosterone axis is typically stimulated in pregnancy. Phaeochromocytoma is a rare cause of hypertension in pregnancy that, if unrecognised, is associated with significant maternal and foetal morbidity and mortality. The diagnosis can be established by measuring levels of catecholamines (noradrenaline and adrenaline) and/or their metabolites (normetanephrine and metanephrine) in plasma or urine.

What Was the Diagnosis?

Catecholamine levels in 24-hour urine collections were found to be markedly raised. Urinary noradrenaline excretion was markedly elevated at 5,659 nmol, 8,225 nmol, and 9,601 nmol/day in repeated collections at 21 weeks of gestation (normal range 63–416 nmol/day). Urinary adrenaline excretion was normal. Pregnancy may induce mild elevation of catecholamine levels, but the marked elevation of urinary catecholamine observed was diagnostic of phaeochromocytoma. Conditions that are associated with false positive results, such as acute myocardial infarction, congestive heart failure, acute cerebrovascular event, withdrawal from alcohol, withdrawal from clonidine, and cocaine abuse, were not present in our patient.

The working diagnosis was therefore phaeochromocytoma complicating pregnancy. Magnetic resonance imaging (MRI) of neck to pelvis, without gadolinium enhancement, was performed at 24 weeks of gestation. It showed a 4.2 cm solid lesion in the mid-abdominal aorto-caval region, while both adrenals were unremarkable. There were no ectopic lesions seen in the rest of the examined areas. Based on existing investigation findings, it was concluded that she had extra-adrenal paraganglioma resulting in hypertension.

What Was the Next Step in Management?

At 22 weeks of gestation, the patient was started on phenoxybenzamine titrated to a dose of 30 mg in the morning and 10 mg in the evening. Propranolol was added several days after the commencement of phenoxybenzamine. Apart from mild postural dizziness, the medical therapy was well tolerated during the remainder of the pregnancy. In the third trimester, systolic and diastolic blood pressures were maintained to below 90 mmHg and 60 mmHg, respectively. During this period, she developed mild elevation of alkaline phosphatase ranging from 91 to 188 IU/l (reference 35–85 IU/l). However, liver transaminases were normal and the patient had no seizures. Repeated urinalysis showed resolution of proteinuria. At 38 weeks of gestation, the patient proceeded to elective caesarean section because of previous caesarean section, and a live female baby weighing 3.14 kg was delivered. The delivery was uncomplicated and blood pressure remained stable.

Following the delivery, computer tomography (CT) scan of neck, abdomen, and pelvis was performed as part of pre-operative planning to better delineate the relationship of the tumour to neighbouring structures. In addition to the previously identified extra-adrenal paraganglioma in the abdomen ( Figure 1 ), the CT revealed a 9 mm hypervascular nodule at the left carotid bifurcation, suggestive of a carotid body tumour ( Figure 2 ). The patient subsequently underwent an iodine (I) 131 metaiodobenzylguanidine (MIBG) scan, which demonstrated marked MIBG-avidity of the paraganglioma in the mid-abdomen. The reported left carotid body tumour, however, did not demonstrate any significant uptake. This could indicate either that the MIBG scan had poor sensitivity in detecting a small tumour, or that the carotid body tumour was not functional.

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https://doi.org/10.1371/journal.pmed.1000037.g001

https://doi.org/10.1371/journal.pmed.1000037.g002

In June 2008, four months after the delivery, the patient had a laparotomy with removal of the abdominal paraganglioma. The operation was uncomplicated. There was no wide fluctuation of blood pressures intra- and postoperatively. Phenoxybenzamine and propranolol were stopped after the operation. Histology of the excised tumour was consistent with paraganglioma with cells staining positive for chromogranin ( Figures 3 and 4 ) and synaptophysin. Adrenal tissues were notably absent.

The tumour is a well-circumscribed fleshy yellowish mass with maximal dimension of 5.5 cm.

https://doi.org/10.1371/journal.pmed.1000037.g003

The tumour cells are polygonal with bland nuclei. The cells are arranged in nests and are immunoreactive to chromogranin (shown here) and synaptophysin.

https://doi.org/10.1371/journal.pmed.1000037.g004

The patient was counselled for genetic testing for hereditary phaeochromocytoma/paraganglioma. She was found to be heterozygous for c.449_453dup mutation of the succinate dehydrogenase subunit D (SDHD) gene ( Figure 5 ). This mutation is a novel frameshift mutation, and leads to SDHD deficiency (GenBank accession number: 1162563). At the latest clinic visit in August 2008, she was asymptomatic and normotensive. Measurements of catecholamine in 24-hour urine collections had normalised. Resection of the left carotid body tumour was planned for a later date. She was to be followed up indefinitely to monitor for recurrences. She was also advised to contact family members for genetic testing. Our patient gave written consent for this case to be published.

https://doi.org/10.1371/journal.pmed.1000037.g005

Phaeochromocytoma in Pregnancy

Hypertension during pregnancy is a frequently encountered obstetric complication that occurs in 6%–8% of pregnancies [ 2 ]. Phaeochromocytoma presenting for the first time in pregnancy is rare, and only several hundred cases have been reported in the English literature. In a recent review of 41 cases that presented during 1988 to 1997, maternal mortality was 4% while the rate of foetal loss was 11% [ 3 ]. Antenatal diagnosis was associated with substantial reduction in maternal mortality but had little impact on foetal mortality. Further, chronic hypertension, regardless of aetiology, increases the risk of pre-eclampsia by 10-fold [ 1 ].

Classically, patients with phaeochromocytoma present with spells of palpitation, headaches, and diaphoresis [ 4 ]. Hypertension may be sustained or sporadic, and is associated with orthostatic blood pressure drop because of hypovolaemia and impaired vasoconstricting response to posture change. During pregnancy, catecholamine surge may be triggered by pressure from the enlarging uterus and foetal movements. In the majority of cases, catecholamine-secreting tumours develop in the adrenal medulla and are termed phaeochromocytoma. Ten percent of tumours arise from extra-adrenal chromaffin tissues located in the abdomen, pelvis, or thorax to form paraganglioma that may or may not be biochemically active. The malignant potential of phaeochromocytoma or paraganglioma cannot be determined from histology and is inferred by finding tumours in areas of the body not known to contain chromaffin tissues. The risk of malignancy is higher in extra-adrenal tumours and in tumours that secrete dopamine.

Making the Correct Diagnosis

The diagnosis of phaeochromocytoma requires a combination of biochemical and anatomical confirmation. Catecholamines and their metabolites, metanephrines, can be easily measured in urine or plasma samples. Day collection of urinary fractionated metanephrine is considered the most sensitive in detecting phaeochromocytoma [ 5 ]. In contrast to sporadic release of catecholamine, secretion of metanephrine is continuous and is less subjective to momentary stress. Localisation of tumour can be accomplished by either CT or MRI of the abdomen [ 6 ]. Sensitivities are comparable, although MRI is preferable in pregnancy because of minimal radiation exposure. Once a tumour is identified, nuclear medicine imaging should be performed to determine its activity, as well as to search for extra-adrenal diseases. I 131 or I 123 MIBG scan is the imaging modality of choice. Metaiodobenzylguanidine structurally resembles noradrenaline and is concentrated in chromaffin cells of phaeochromocytoma or paraganglioma that express noradrenaline transporters. Radionucleotide imaging is contraindicated in pregnancy and should be deferred until after the delivery.

Treatment Approach

Upon confirming the diagnosis, medical therapy should be initiated promptly to block the cardiovascular effects of catecholamine release. Phenoxybenzamine is a long-acting non-selective alpha-blocker commonly used in phaeochromocytoma to control blood pressure and prevent cardiovascular complications [ 7 ]. The main side-effects of phenoxybenzamine are postural hypotension and reflex tachycardia. The latter can be circumvented by the addition of a beta-blocker. It is important to note that beta-blockers should not be used in isolation, since blockade of ß2-adrenoceptors, which have a vasodilatory effect, can cause unopposed vasoconstriction by a1-adrenoceptor stimulation and precipitate severe hypertension. There is little data on the safety of use of phenoxybenzamine in pregnancy, although its use is deemed necessary and probably life-saving in this precarious situation.

The definitive treatment of phaeochromocytoma or paraganglioma is surgical excision. The timing of surgery is critical, and the decision must take into consideration risks to the foetus, technical difficulty regarding access to the tumour in the presence of a gravid uterus, and whether the patient's symptoms can be satisfactorily controlled with medical therapy [ 8 , 9 ]. It has been suggested that surgical resection is reasonable if the diagnosis is confirmed and the tumour identified before 24 weeks of gestation. Otherwise, it may be preferable to allow the pregnancy to progress under adequate alpha- and beta-blockade until foetal maturity is reached. Unprepared delivery is associated with a high risk of phaeochromocytoma crisis, characterised by labile blood pressure, tachycardia, fever, myocardial ischaemia, congestive heart failure, and intracerebral bleeding.

Patients with phaeochromocytoma or paraganglioma should be followed up for life. The rate of recurrence is estimated to be 2%–4% at five years [ 10 ]. Assessment for recurrent disease can be accomplished by periodic blood pressure monitoring and 24-hour urine catecholamine and/or metanephrine measurements.

Genetics of Phaeochromocytoma

Approximately one quarter of patients presenting with phaeochromocytoma may carry germline mutations, even in the absence of apparent family history [ 11 ]. The common syndromes of hereditary phaeochromocytoma/paraganglioma are listed in Box 2 . These include Von Hippel-Lindau syndrome, multiple endocrine neoplasia type 2, neurofibromatosis type 1, and succinate dehydrogenase (SDH) gene mutations. Our patient has a novel frameshift mutation in the SDHD gene located at Chromosome 11q. SDH is a mitochondrial enzyme that is involved in oxidative phosphorylation. Characteristically, SDHD mutation is associated with head or neck non-functional paraganglioma, and infrequently, sympathetic paraganglioma or phaeochromocytoma [ 12 ]. Tumours associated with SDHD mutation are rarely malignant, in contrast to those arisen from mutation of the SDHB gene. Like all other syndromes of hereditary phaeochromocytoma, SDHD mutation is transmitted in an autosomal dominant fashion. However, not all carriers of the SDHD mutation develop tumours, and inheritance is further complicated by maternal imprinting in gene expression. While it may not be practical to screen for genetic alterations in all cases of phaeochromocytoma, most authorities advocate genetic screening for patients with positive family history, young age of tumour onset, co-existence with other neoplasms, bilateral phaeochromocytoma, and extra-adrenal paraganglioma. The confirmation of genetic mutation should prompt evaluation of other family members.

Box 2: Hereditary Phaeochromocytoma/Paraganglioma Syndromes

• Von Hippel-Lindau syndrome
• Multiple endocrine neoplasia type 2A and type 2B
• Neurofibromatosis type 1
• Mutation of SDHB , SDHC , SDHD
• Ataxia-telangiectasia
• Tuberous sclerosis
• Sturge-Weber syndrome

Key Learning Points

• Hypertension complicating pregnancy is a commonly encountered medical condition.
• Pre-existing chronic hypertension must be considered in patients with hypertension presenting in pregnancy, particularly if elevation of blood pressure is detected early during pregnancy or if persists post-partum.
• Secondary causes of chronic hypertension include renal artery stenosis, renal parenchyma disease, primary hyperaldosteronism, phaeochromocytoma, Cushing's syndrome, coarctation of the aorta, and obstructive sleep apnoea.
• Phaeochromocytoma presenting during pregnancy is rare but carries high rates of maternal and foetal morbidity and mortality if unrecognised.
• Successful outcomes depend on early disease identification, prompt initiation of alpha- and beta-blockers, carefully planned delivery, and timely resection of the tumour.

Phaeochromocytoma complicating pregnancy is uncommon. Nonetheless, in view of the potential for catastrophic consequences if unrecognised, a high index of suspicion and careful evaluation for secondary causes of hypertension is of utmost importance. Blood pressure should be monitored in the post-partum period and persistence of hypertension must be thoroughly investigated.

Author Contributions

All authors participated in the management of the patient or writing of the article. AL and RCWM wrote the article, with contributions from all the authors.

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Case study: 60-year-old female presenting with shortness of breath.

Deepa Rawat ; Sandeep Sharma .

Affiliations

Last Update: February 20, 2023 .

• Case Presentation

The patient is a 60-year-old white female presenting to the emergency department with acute onset shortness of breath.  Symptoms began approximately 2 days before and had progressively worsened with no associated, aggravating, or relieving factors noted. She had similar symptoms approximately 1 year ago with an acute, chronic obstructive pulmonary disease (COPD) exacerbation requiring hospitalization. She uses BiPAP ventilatory support at night when sleeping and has requested to use this in the emergency department due to shortness of breath and wanting to sleep.

She denies fever, chills, cough, wheezing, sputum production, chest pain, palpitations, pressure, abdominal pain, abdominal distension, nausea, vomiting, and diarrhea.

She reports difficulty breathing at rest, forgetfulness, mild fatigue, feeling chilled, requiring blankets, increased urinary frequency, incontinence, and swelling in her bilateral lower extremities that are new-onset and worsening. Subsequently, she has not ambulated from bed for several days except to use the restroom due to feeling weak, fatigued, and short of breath.

There are no known ill contacts at home. Her family history includes significant heart disease and prostate malignancy in her father. Social history is positive for smoking tobacco use at 30 pack years. She quit smoking 2 years ago due to increasing shortness of breath. She denies all alcohol and illegal drug use. There are no known foods, drugs, or environmental allergies.

Past medical history is significant for coronary artery disease, myocardial infarction, COPD, hypertension, hyperlipidemia, hypothyroidism, diabetes mellitus, peripheral vascular disease, tobacco usage, and obesity.  Past surgical history is significant for an appendectomy, cardiac catheterization with stent placement, hysterectomy, and nephrectomy.

Her current medications include fluticasone-vilanterol 100-25 mcg inhaled daily, hydralazine 50 mg by mouth, 3 times per day, hydrochlorothiazide 25 mg by mouth daily, albuterol-ipratropium inhaled every 4 hours PRN, levothyroxine 175 mcg by mouth daily, metformin 500 mg by mouth twice per day, nebivolol 5 mg by mouth daily, aspirin 81 mg by mouth daily, vitamin D3 1000 units by mouth daily, clopidogrel 75 mg by mouth daily, isosorbide mononitrate 60 mg by mouth daily, and rosuvastatin 40 mg by mouth daily.

Physical Exam

Initial physical exam reveals temperature 97.3 F, heart rate 74 bpm, respiratory rate 24, BP 104/54, HT 160 cm, WT 100 kg, BMI 39.1, and O2 saturation 90% on room air.

Constitutional:  Extremely obese, acutely ill-appearing female. Well-developed and well-nourished with BiPAP in place. Lying on a hospital stretcher under 3 blankets.

HEENT: 

• Head: Normocephalic and atraumatic
• Mouth: Moist mucous membranes 
• Macroglossia
• Eyes: Conjunctiva and EOM are normal. Pupils are equal, round, and reactive to light. No scleral icterus. Bilateral periorbital edema present.
• Neck: Neck supple. No JVD present. No masses or surgical scarring. 
• Throat: Patent and moist

Cardiovascular:  Normal rate, regular rhythm, and normal heart sound with no murmur. 2+ pitting edema bilateral lower extremities and strong pulses in all four extremities.

Pulmonary/Chest:  No respiratory status distress at this time, tachypnea present, (+) wheezing noted, bilateral rhonchi, decreased air movement bilaterally. The patient was barely able to finish a full sentence due to shortness of breath.

Abdominal:  Soft. Obese. Bowel sounds are normal. No distension and no tenderness

Skin: Skin is very dry

Neurologic: Alert, awake, able to protect her airway. Moving all extremities. No sensation losses

• Initial Evaluation

Initial evaluation to elucidate the source of dyspnea was performed and included CBC to establish if an infectious or anemic source was present, CMP to review electrolyte balance and review renal function, and arterial blood gas to determine the PO2 for hypoxia and any major acid-base derangement, creatinine kinase and troponin I to evaluate the presence of myocardial infarct or rhabdomyolysis, brain natriuretic peptide, ECG, and chest x-ray. Considering that it is winter and influenza is endemic in the community, a rapid influenza assay was obtained as well.

Largely unremarkable and non-contributory to establish a diagnosis.

Showed creatinine elevation above baseline from 1.08 base to 1.81, indicating possible acute injury. EGFR at 28 is consistent with chronic renal disease. Calcium was elevated to 10.2. However, when corrected for albumin, this corrected to 9.8 mg/dL. Mild transaminitis is present as seen in alkaline phosphatase, AST, and ALT measurements which could be due to liver congestion from volume overload.

Initial arterial blood gas with pH 7.491, PCO2 27.6, PO2 53.6, HCO3 20.6, and oxygen saturation 90% on room air, indicating respiratory alkalosis with hypoxic respiratory features.

Creatinine kinase was elevated along with serial elevated troponin I studies. In the setting of her known chronic renal failure and acute injury indicated by the above creatinine value, a differential of rhabdomyolysis is determined.

Influenza A and B: Negative

Normal sinus rhythm with non-specific ST changes in inferior leads. Decreased voltage in leads I, III, aVR, aVL, aVF.

Chest X-ray

Findings: Bibasilar airspace disease that may represent alveolar edema. Cardiomegaly noted. Prominent interstitial markings were noted. Small bilateral pleural effusions

Radiologist Impression: Radiographic changes of congestive failure with bilateral pleural effusions greater on the left compared to the right

• Differential Diagnosis
• Acute on chronic COPD exacerbation
• Acute on chronic renal failure
• Bacterial pneumonia
• Congestive heart failure
• Pericardial effusion
• Hypothyroidism
• Influenza pneumonia
• Pulmonary edema
• Pulmonary embolism
• Confirmatory Evaluation

On the second day of the admission patient’s shortness of breath was not improved, and she was more confused with difficulty arousing on conversation and examination. To further elucidate the etiology of her shortness of breath and confusion, the patient's husband provided further history. He revealed that she is poorly compliant with taking her medications. He reports that she “doesn’t see the need to take so many pills.”

Testing was performed to include TSH, free T4, BNP, repeated arterial blood gas, CT scan of the chest, and echocardiogram. TSH and free T4 evaluate hypothyroidism. BNP evaluates fluid load status and possible congestive heart failure. CT scan of the chest will look for anatomical abnormalities. An echocardiogram is used to evaluate left ventricular ejection fraction, right ventricular function, pulmonary artery pressure, valvular function, pericardial effusion, and any hypokinetic area.

• TSH: 112.717 (H)
• Free T4: 0.56 (L)
• TSH and Free T4 values indicate severe primary hypothyroidism. 

BNP can be falsely low in obese patients due to the increased surface area. Additionally, adipose tissue has BNP receptors which augment the true BNP value. Also, African American patients with more excretion may have falsely low values secondary to greater excretion of BNP. This test is not that helpful in renal failure due to the chronic nature of fluid overload. This allows for desensitization of the cardiac tissues with a subsequent decrease in BNP release.

Repeat arterial blood gas on BiPAP ventilation shows pH 7.397, PCO2 35.3, PO2 72.4, HCO3 21.2, and oxygen saturation 90% on 2 L supplemental oxygen.

CT chest without contrast was primarily obtained to evaluate the left hemithorax, especially the retrocardiac area.

Radiologist Impression: Tiny bilateral pleural effusions. Pericardial effusion. Coronary artery calcification. Some left lung base atelectasis with minimal airspace disease.

Echocardiogram

The left ventricular systolic function is normal. The left ventricular cavity is borderline dilated.

The pericardial fluid is collected primarily posteriorly, laterally but not apically. There appeared to be a subtle, early hemodynamic effect of the pericardial fluid on the right-sided chambers by way of an early diastolic collapse of the RA/RV and delayed RV expansion until late diastole. A dedicated tamponade study was not performed. 

The estimated ejection fraction appears to be in the range of 66% to 70%. The left ventricular cavity is borderline dilated.

The aortic valve is abnormal in structure and exhibits sclerosis.

The mitral valve is abnormal in structure. Mild mitral annular calcification is present. There is bilateral thickening present. Trace mitral valve regurgitation is present.

• Myxedema coma or severe hypothyroidism
• Pericardial effusion secondary to myxedema coma
• COPD exacerbation
• Acute on chronic hypoxic respiratory failure
• Acute respiratory alkalosis
• Bilateral community-acquired pneumonia
• Small bilateral pleural effusions
• Acute mild rhabdomyolysis
• Acute chronic, stage IV, renal failure
• Elevated troponin I levels, likely secondary to Renal failure 
• Diabetes mellitus type 2, non-insulin-dependent
• Extreme obesity
• Hepatic dysfunction

The patient was extremely ill and rapidly decompensating with multisystem organ failure, including respiratory failure, altered mental status, acute on chronic renal failure, and cardiac dysfunction. The primary concerns for the stability of the patient revolved around respiratory failure coupled with altered mental status. In the intensive care unit (ICU), she rapidly began to fail BiPAP therapy. Subsequently, the patient was emergently intubated in the ICU.  A systemic review of therapies and hospital course is as follows:

Considering the primary diagnosis of myxedema coma, early supplementation with thyroid hormone is essential. Healthcare providers followed the American Thyroid Association recommendations, which recommend giving combined T3 and T4 supplementation; however, T4 alone may also be used. T3 therapy is given as a bolus of 5 to 20 micrograms intravenously and continued at 2.5 to 10 micrograms every 8 hours. An intravenous loading dose of 300 to 600 micrograms of T4 is followed by a daily intravenous dose of 50 to 100 micrograms. Repeated monitoring of TSH and T4 should be performed every 1 to 2 days to evaluate the effect and to titrate the dose of medication. The goal is to improve mental function. Until coexistent adrenal insufficiency is ruled out using a random serum cortisol measurement, 50 to 100 mg every 8 hours of hydrocortisone should be administered. In this case, clinicians used hydrocortisone 100 mg IV every 8 hours. Dexamethasone 2 to 4 mg every 12 hours is an alternative therapy.

The patient’s mental status rapidly worsened despite therapy. In the setting of her hypothyroidism history, this may be myxedema coma or due to the involvement of another organ system. The thyroid supplementation medications and hydrocortisone were continued. A CT head without contrast was normal.

Respiratory

For worsening metabolic acidosis and airway protection, the patient was emergently intubated. Her airway was deemed high risk due to having a large tongue, short neck, and extreme obesity. As the patient’s heart was preload dependent secondary to pericardial effusion, a 1-liter normal saline bolus was started. Norepinephrine was started at a low dose for vasopressor support, and ketamine with low dose Propofol was used for sedation. Ketamine is a sympathomimetic medication and usually does not cause hypotension as all other sedatives do. The patient was ventilated with AC mode of ventilation, tidal volume of 6 ml/kg ideal body weight, flow 70, initial fio2 100 %, rate 26 per minute (to compensate for metabolic acidosis), PEEP of 8.

Cardiovascular

She was determined to be hemodynamically stable with a pericardial effusion. This patient’s cardiac dysfunction was diastolic in nature, as suggested by an ejection fraction of 66% to 70%. The finding of posterior pericardial effusion further supported this conclusion. The posterior nature of this effusion was not amenable to pericardiocentesis. As such, this patient was preload dependent and showed signs of hypotension. The need for crystalloid fluid resuscitation was balanced against the impact increased intravascular volume would have on congestive heart failure and fluid overload status. Thyroid hormone replacement as above should improve hypotension. However, vasopressor agents may be used to maintain vital organ perfusion targeting a mean arterial pressure of greater than 65 mm Hg as needed. BP improved after fluid bolus, and eventually, the norepinephrine was stopped. Serial echocardiograms were obtained to ensure that the patient did not develop tamponade physiology. Total CK was elevated, which was likely due to Hypothyroidism compounded with chronic renal disease.

Infectious Disease

Blood cultures, urine analysis, and sputum cultures were obtained. The patient's white blood cell count was normal. This is likely secondary to her being immunocompromised due to hypothyroidism and diabetes. In part, the pulmonary findings of diffuse edema and bilateral pleural effusions can be explained by cardiac dysfunction. Thoracentesis of pleural fluid was attempted, and the fluid was analyzed for cytology and gram staining to rule out infectious or malignant causes as both a therapeutic and diagnostic measure. Until these results return, broad-spectrum antibiotics are indicated and may be discontinued once the infection is ruled out completely.

Gastrointestinal

Nasogastric tube feedings were started on the patient after intubation. She tolerated feedings well. AST and ALT were mildly elevated, which was thought to be due to hypothyroidism, and as the TSH and free T4 improved, her AST and ALT improved. Eventually, these values became normal once her TSH level was close to 50.

Her baseline creatinine was found to be close to 1.08 in prior medical records. She presented with a creatinine of 1.8 in the emergency department. Since hypothyroidism causes fluid retention in part because thyroid hormone encourages excretion of free water and partly due to decreased lymphatic function in returning fluid to vascular circulation.  Aggressive diuresis was attempted. As a result, her creatinine increased initially but improved on repeated evaluation, and the patient had a new baseline creatinine of 1.6. Overall she had a net change in the fluid status of 10 liters negative by her ten days of admission in the ICU.

Mildly anemic otherwise, WBC and platelet counts were normal. Electrolyte balance should be monitored closely, paying attention to sodium, potassium, chloride, and calcium specifically as these are worsened in both renal failure and myxedema. 

Daily sedation vacations were enacted, and the patient's mental status improved and was much better when TSH was around 20. The bilateral pleural effusions improved with aggressive diuresis. Breathing trials were initiated when the patient's fio2 requirements decreased to 60% and a PEEP of 8. She was eventually extubated onto BiPAP and then high-flow nasal cannula while off of BiPAP. Pericardial fluid remained stable, and no cardiac tamponade pathology developed. As a result, it was determined that a pericardial window was unnecessary. Furthermore, she was not a candidate for pericardiocentesis as the pericardial effusion was located posterior to the heart. Her renal failure improved with improved cardiac function, diuretics, and thyroid hormone replacement.

After extubation patient had speech and swallow evaluations and was able to resume an oral diet. The patient was eventually transferred out of the ICU to the general medical floor and eventually to a rehabilitation unit.

Despite the name myxedema coma, most patients will not present in a coma status. This illness is at its core a severe hypothyroidism crisis that leads to systemic multiorgan failure. Thyroid hormones T3, and to a lesser extent, T4 act directly on a cellular level to upregulate all metabolic processes in the body. Therefore, deficiency of this hormone is characterized by systemic decreased metabolism and decreased glucose utilization along with increased production and storage of osmotically active mucopolysaccharide protein complexes into peripheral tissues resulting in diffuse edema and swelling of tissue. [1]

Myxedema coma is an illness that occurs primarily in females at a rate of 4:1 compared to men. It typically impacts the elderly at the age of greater than 60 years old, and approximately 90% of cases occur during the winter months. Myxedema coma is the product of longstanding unidentified or undertreated hypothyroidism of any etiology. Thyroid hormone is necessary throughout the body and acts as a regulatory hormone that affects many organ systems. [2] In cardiac tissues, myxedema coma manifests as decreased contractility with subsequent reduction in stroke volume and overall cardiac output.  Bradycardia and hypotension are typically present also. Pericardial effusions occur due to the accumulation of mucopolysaccharides in the pericardial sac, which leads to worsened cardiac function and congestive heart failure from diastolic dysfunction. Capillary permeability is also increased throughout the body leading to worsened edema. Electrocardiogram findings may include bradycardia and low-voltage, non-specific ST waveform changes with possible inverted T waves.

Neurologic tissues are impacted in myxedema coma leading to the pathognomonic altered mental status resulting from hypoxia and decreased cerebral blood flow secondary to cardiac dysfunction as above. Additionally, hypothyroidism leads to decreased glucose uptake and utilization in neurological tissue, thus worsening cognitive function.

The pulmonary system typically manifests this disease process through hypoventilation secondary to the central nervous system (CNS) depression of the respiratory drive with blunting of the response to hypoxia and hypercapnia. Additionally, metabolic dysfunction in the muscles of respiration leads to respiratory fatigue and failure, macroglossia from mucopolysaccharide driven edema of the tongue leads to mechanical obstruction of the airway, and obesity hypoventilation syndrome with the decreased respiratory drive as most hypothyroid patients suffer from obesity.

Renal manifestations include decreased glomerular filtration rate from the reduced cardiac output and increased systemic vascular resistance coupled with acute rhabdomyolysis lead to acute kidney injury. In the case of our patient above who has a pre-existing renal disease status post-nephrectomy, this is further worsened.  The net effect is worsened fluid overload status compounding the cardiac dysfunction and edema. [3]

The gastrointestinal tract is marked by mucopolysaccharide-driven edema as well leading to malabsorption of nutrients, gastric ileus, and decreased peristalsis. Ascites is common because of increased capillary permeability in the intestines coupled with coexistent congestive heart failure and congestive hepatic failure. Coagulopathies are common to occur as a result of this hepatic dysfunction.

Evaluation: The diagnosis of myxedema coma, as with all other diseases, is heavily reliant on the history and physical exam. A past medical history including hypothyroidism is highly significant whenever decreased mental status or coma is identified. In the absence of identified hypothyroidism, myxedema coma is a diagnosis of exclusion when all other sources of coma have been ruled out. If myxedema coma is suspected, evaluation of thyroid-stimulating hormone (TSH), free thyroxine (T4), and serum cortisol is warranted. T4 will be extremely low. TSH is variable depending on the etiology of hypothyroidism, with a high TSH indicating primary hypothyroidism and a low or normal TSH indicating secondary etiologies. Cortisol may be low indicating adrenal insufficiency because of hypothyroidism.  [4]

Prognosis: Myxedema coma is a medical emergency. With proper and rapid diagnosis and initiation of therapy, the mortality rate is still as high as 25% to 50%. The most common cause of death is due to respiratory failure. The factors which suggest a poorer prognosis include increased age, persistent hypothermia, bradycardia, low score Glasgow Coma Scale, or multi-organ impairment indicated by high APACHE (Acute Physiology and Chronic Health Evaluation) II score. For these reasons, placement in an intensive care unit with a low threshold for intubation and mechanical ventilation can improve mortality outcomes. [3] [5]

• Pearls of Wisdom
• Not every case of shortness of breath is COPD or congestive heart failure (CHF). While less likely, a history of hypothyroidism should raise suspicion of myxedema coma in a patient with any cognitive changes.
• Myxedema is the great imitator illness that impacts all organ systems. It can easily be mistaken for congestive heart failure, COPD exacerbation, pneumonia, renal injury or failure, or neurological insult.
• Initial steps in therapy include aggressive airway management, thyroid hormone replacement, glucocorticoid therapy, and supportive measures.
• These patients should be monitored in an intensive care environment with continuous telemetry. [6]
• Enhancing Healthcare Team Outcomes

This case demonstrates how all interprofessional healthcare team members need to be involved in arriving at a correct diagnosis, particularly in more challenging cases such as this one. Clinicians, specialists, nurses, pharmacists, laboratory technicians all bear responsibility for carrying out the duties pertaining to their particular discipline and sharing any findings with all team members. An incorrect diagnosis will almost inevitably lead to incorrect treatment, so coordinated activity, open communication, and empowerment to voice concerns are all part of the dynamic that needs to drive such cases so patients will attain the best possible outcomes.

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Case Study of 60 year old female presenting with Shortness of Breath Contributed by Sandeep Sharma, MD

Disclosure: Deepa Rawat declares no relevant financial relationships with ineligible companies.

Disclosure: Sandeep Sharma declares no relevant financial relationships with ineligible companies.

This book is distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ), which permits others to distribute the work, provided that the article is not altered or used commercially. You are not required to obtain permission to distribute this article, provided that you credit the author and journal.

• Cite this Page Rawat D, Sharma S. Case Study: 60-Year-Old Female Presenting With Shortness of Breath. [Updated 2023 Feb 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.

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