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The Importance of Understanding Hypertension: The Role of a Registered Nurse as an Investigator 

The Importance of Understanding Hypertension: The Role of a Registered Nurse as an Investigator by Gary D. Goldberg, PhD Clinical Professor of Medical Education Angeles College of Nursing, Los Angeles, Ca. [email protected]


  Hypertension is a chronic medical ‘condition’ in which the blood pressure is elevated. Hypertension also, referred to as high blood pressure, (i.e., HT, HTN or HPN). The word “Hypertension” (i.e., elevation within the circulatory system) and by itself refers to a systemic, arterial hypertension.

  Hypertension by definition has been classified as ‘essential and/or idiopathic,’ 1 (i.e., primary or secondary concerning metabolic syndrome), multiplex risk factors for cardiovascular disease (CVD) or Syndrome X.2 Primary HTN means that no medical or scientific cause was notable, to explain the raised blood pressure. Metabolic syndrome is a major growing concern among physicians and nursing practitioners’ working in the emergency room department and outpatient clinics. Today, Syndrome X has been placed on the primary essential assessment list for new patients that have no known history for cause. In addition, Syndrome X has become common among the younger adults in the United States since 2000.3  About 90-95% of HT is ‘essential hypertension.’ Secondary HT too, indicates high blood pressure because of, (i.e., Secondary to another condition, such as pathophysiology, metabolic or abnormal organ function). For example, chronic kidney functions, liver, cardiovascular, or tumor diseases.
Keywords: essential hypertension, syndrome x, persistent hypertension, , un-spoken-evidence-based practice, markedly elevated in the chronic state, initial observation, in the state of etiology, the goal of treatment should be in B/P control.

  Today, we need to have a better understanding of “persistent hypertension” which is a key component and a high risk factor for strokes, (i.e., CVA, heart attacks, i.e., Ac³MI, heart failure, i.e., CHF, and arterial aneurysm, i.e., AA). In addition, HTN is indeed a leading cause of chronic renal failure in the United States.4 Even with moderate elevation, in arterial blood pressure well lead to a shortened life expectancy. In the cause of severer high blood pressure, (i.e., B/P as defined as mean arterial pressure 50% or more above average), a person can expect to live no more than a few years unless appropriately treated.5 

  All registered nurses learn that the beginning of a systolic pressure represents (i.e., at peak pressure in the arteries), which occurs near the end of the cardiac cycle, when the ventricles are contracting @ 115 mmHg. Also, the diastolic pressure (i.e., which is minimum pressure in the arteries), occurs near the beginning of the cardiac cycle when the ventricles are filled with blood @ 75 mmHg. Sometimes noted as 115/75 mmHg. Cardiovascular disease (CVD) risk will double for each increment of 20/10 mmHg factor.6 

  The practitioner or primary care nurse’s role will continue to evolve with the focus of patient care moving from ‘secondary care to prime investigator.’ In today’s highly specialized medical care practice, the nurses are taking the lead role in chronic disease management such as diabetes, respiratory conditions and of hypertension disorder. Indeed, to run this nursing-based-management safely, nurses must have the necessary knowledge and skills in accordance with the American Heart Guidelines and the American Nursing Association is backing for code of conduct. In the UK today the governing guidelines are set forth through the NMC code of conduct;7,8 the guidelines are not only to protect the nurse’s but also the patients who are in treatment. It is highly important and vital to the success of ‘nurse-led-clinics’ that an agreed set of guidelines are developed and a framework is maintained , and reviewed on a regular basis between the physician’s group practice and the nurses.

  A current classification through the American Heart Association , Scientific Division (AHA), recommends blood pressure criteria for defining: normal range, pre-hypertension, hypertension (stage I and II), and isolated systolic hypertension,9 which is common among the elderly. The clinical studies are based on the average of ‘seated’ B/P readings that were properly measured during two or more office visits. In individuals older than 50 years of age, according to AHA guidelines, HTN is considered present when a patient’s B/P is consistently are at least 140-mmHg systolic or 90 mmHg diastolic. Patients with B/P over 130/80 mmHg along with Type 1 or Type 2 diabetes, or kidney disease will require further treatment.10

CLASS Systolic pressure Diastolic pressure
  mmHg kPa (kN/m2) mmHg kPa (kN/m2
Normal 90-119 12-15.9 60-79 8.0-10.5
Pre-HTN 120-139 16.0-18.5 80-89 10.7-11.9
Stage 1 140-159 18.7-21.2 90-99 12.0-13.2
Stage 2 > 160 > 21.3 > 100 > 13.3
Isolated systolic HTN > 140 > 18.7 <90 <12.0
Note: The Amer. H. Assoc.
  The registered nurse must start his and/or her investigation even before the patient takes a set in the triage room and before the first question asked. The “art” and “science,” of the un-spoken evidence-based-practice of nursing, is identifying through the signs and symptoms in observation and articulation.


  Some of the evidence may show an accelerated HPN in association with chronic headaches, somnolence, confusion state, visual disturbances, and nausea with vomiting (i.e., hypertensive encephalopathy). Also, note the retinas sometimes appear effected with narrowing of arterial diameter to less than 50% of venous diameter, copper and/or silver wire appearance, exudates, hemorrhages, or papilledema.11 Some signs and symptoms are important among infants and neo-nates such as ‘failure to thrive,’ associated with seizure, irritability or lethargy, and respiratory distress.12 Also, in children (6-16 years of age), HPN may manifest itself through strong headaches, chronic fatigue, intermittent blurred vision, epistaxis, i.e. nosebleed, and through bell-palsy disorder.13

  Another important clue, sign and/or symptom for the practitioner to investigate would be a secondary medical cause of chronic (i.e., 12 weeks or longer) HPN, such as centripetal obesity, “buffalo hump,” and/or wide purple abnormal striae and maybe a recent onset of diabetes could suggest glucocorticoid excess due to either Cushing’s syndrome or other causes. Cushing’s syndrome, hits young to middle-age adults ages 20-50, with signs such as wasting of muscles, thinning of the skin, severe fatigue, high B/P, hyperglycemia (high blood sugar), and weakened bones.14 Also, HPN has been associated with other secondary endocrine diseases such as hyperthyroidism, hypothyroidism, or growth hormone excess shows symptoms specific to these disease such as in hyperthyroidism there may be weight loss, tremor disorder, tachycardia, or atrial arrhythmia, palmar erythema (i.e., reddening of the palms) plus, 30% of patients with rheumatoid arthritis show signs. In addition, an onset of persistent sweating may accrue.15 
  The registered nurse should note with high B/P by asking if the patient has or is having angina or augmenting acute pulmonary edema. This could be a doll or quick sharp pain from the neck, down through one or both arms. The onset could last just a few moments and have no lasting effects. When B/P is markedly elevated in the chronic state, untreated could lead to left ventricular hypertrophy (i.e., LVH), which can present with exertional and paroxysmal nocturnal dyspnea.16 LVH is a major risk factor for cardiovascular morbidity in HTN patients. The effects of diuretics on LVH have raised controversies, but recent studies suggest that diuretics are able to reduce LVH in hypertensive patients, mainly through a reduction in ventricular diameter.17 Also, note with chronic HPN the possibility of cerebral involvement could cause stroke (i.e., CVA), due to thrombosis or hemorrhage from microaneurysms of small penetrating intracranial arteries. HTN encephalopathy could cause an acute capillary congestion and exudation with cerebral edema, which is reversible.18 

Initial Observation- 
  Please understand that as a practicing nurse, you should never be lulled into believing that all patients are the same. Therefore, ‘a blanket approach’ to HTN management, may be used. Below, are some guidelines to help you get started with developing your own initial assessments for uses in hospitals and/or clinic setting:

Baseline approach: Systolic B/P of >160 mmHg

Baseline approach: Diastolic B/P of <100 mmHg

Background symptoms suggestive of secondary causes of HPN, (e.g., renal stenosis)…
Check for family history of Cardio activities, i.e. unstable angina, palpitations, chest discomfort, heart disease, or valvular stenosis…
Past history of cerebrovascular trauma, or accident, (i.e., head injury, fall, and swelling in extremities’), car or mechanical devise indent…
Diabetes Mellitus Type 2, (i.e., adult onset)…
Hyperlipidaemia, (i.e., group of abnormal elevated levels of lipids (fats) in the blood)…
Smoking status and how much…
Drug history, (e.g., oral contraceptives), cyclosporine (immunosuppressant) given with kidney disease, Crohn disease, and aplastic anemia (shortages of red & white blood cells)…
Lifestyle: salt and fat intakes…

Initial Physical examination- 
Take a reading of the body mass index (BMI)…
Chest examination, check for evidence of heart failure (HF) in patients presenting with associated shortness of breath (SOB)…
Cardiovascular disease or electro-physiology disorders, i.e. particularly look for left ventricular hypertrophy (LVH), arterial bruits or heart murmur sounds (S₁, S₂, S₃)…
Check abdomen for bruits, also, enlarged kidneys and/or other masses present…
Check for fundi oculi, (i.e., yellowing nails), also affects the interior of the eye wall…
Initial investigation for acute (Ac3) diagnosed HPN- 
Include a blood test for urea and electrolytes, glucose, lipid panel, complete blood count (CBC). In addition, creatinine (BUN) and estimated glomerular filtration rate (eGFR)…
Urinalysis for glucose and protein…
Order an ECG: this cardio-diagnostic tool can detect LVH (sum of the S-wave in lead V₁ or V₂ and the R-wave in V₅ or V₆ >mm or atrial fibrillation (AF), (i.e., no visible P-waves are essentially normal, QRS waves are occurring at irregular intervals).
Also, if your patient has a history of pulmonary hypertension and/or CHF, have the clinicians’ order an 2-D Echocardiograph with Color Flow Doppler, for a possible abnormal ejection fraction.19 Due to chronic, (i.e., 12 weeks or longer) elevation in pulmonary pressures, the clinical findings are usually based on several pieces of data. Symptoms, echocardiogram, and if necessary, a right heart catheterization.
As a nurse, your communication skills, are an important factor when obtaining a thorough history from the patient and may lead to identifying a ‘remarkable feature, ’regarding the patient’s condition. As noted, by Aminoff and Kjellgren, et. al., (2001), 20,21 and observation puts both nurses and physicians’ in a ‘check and balance’ relationship, which is for the greater in identifying physical and social, (i.e., lifestyle issues).
In observation, the patients have longer conversations with nurses than physicians do.
Registered nurses will talk with patients about other vascular risk factors more frequently than physicians do.
Doctor-patient consultations tend to be medication and/or physiological focused, (i.e., evidenced-based).
Patients tend to raise more topics with nurses than physicians. One may suggest that nurses articulate with understanding by every-day patients. There may be common ground between nurses-to-patients and this could lead to a full humanity approach between the ‘art and science’ in reaching a medical conclusion.
In addition, it is vital that adequate time allowed completing an assessment for HTP. According to the Nurses’ Hypertension Association, suggests that the initial appointment time of 30 minutes to assess cardiovascular history and give both dietary and lifestyle advice, while an annual review should allot, between 15-20 minutes.
Note:  Arterial pressure fluctuates in most people, whether they are normotensive or hypertensive. Some patients will be classified, as having labile hypertension are those who sometimes, but not always, have arterial pressures in the hypertensive range. These patients are often considered to have borderline HTN.
  Another important symptom for the registered nurse to identify during a women’s pregnancy (high or fluctuating B/P), would be the possibility of pre-eclampsia and eclampsia.22 There usually appear swelling at the extremities and extreme joint pain. Edema is one of the hallmarks of eclampsia, which is convulsion. The other signs may precede the convulsion such as nausea, vomiting, headaches, and in extreme matters, blindness.23 


  In the state of etiology (i.e., origin of disease), as secondary HPN differs widely amongst individuals within a large population setting. The term ‘essential hypertension’ is the form of HPN that by definition has no identifiable cause. Some studies suggest that HPN relates to the aging process24 and to some inherited genetic mutations.25 Renin, (i.e., angiotensin antagonist, an enzyme) released into the blood by the kidney in response to stress.26 Too much renin can cause a condition called ‘renal vascular hypertension’. HPN patients with low-baseline ‘plasma renin activity’ (PRA) are known to respond best to natriuretic drugs, and those with high PRA respond best to rein-angiotensin system (RAS) blockade. However, there has been recent speculation that B/P-lowering response to the renin inhibitor, Aliskiren or by trade name Tekturna, (i.e., renin inhibitor for hepatic or renal function impairment). This might be blunted in some patients with medium-to high baseline PRA.27 

  Obtaining reliable B/P measurements relies on following several rules and understanding the many factors that influence B/P readings. For example, the measurements in control of HPN should be at least one hour after caffeine consumption, and for smokers, thirty minutes after their last smoke or strenuous exercise plus without any stress. The cuff size is also important issue. The bladder should encircle and cover two-thirds of the length of the upper arm. The patient should be sitting upright in a chair with both feet flat on the floor or mat for a minimum time of five minutes prior to taking the reading. In addition, the patient should not be on any adrenergic stimulants, such as those found in many cold medications.

Another important observation for the registered nurse to keep in mind is many patients demonstrate “white-coat-hypertension or (WCH).” A phenomenon in which patient’s exhibit elevated B/P in a clinical setting but not when recorded by themselves at home. It is understood today that this is due to ‘anxiety’ in some patients experience during a clinic visit. Patients of white-coat-hypertension do not exhibit the signs indicative of trepidation and their increased B/P does not often accompanied with symptoms such as tachycardia or an irregular heart rhythm. Studies have shown repeatedly that 15-30% of those patients thought to have mild HPN because of clinic or an office recording,28 display normal range B/P, and show little to no unusual response to pressure stimulus.


  Concerning talking manual measurements, the nurse taking the measurement should be careful to inflate the cuff suitably above anticipated systolic pressure. Taking your stethoscope and placing it over the brachial artery, and making sure that arm is at the level of the heart and the cuff deflates at a rate of 2 to 3 mmHg/s.29 In the elderly patients who particularly when treated may show ‘orthostatic hypotension,’ measuring lying sitting and standing B/P may indeed be useful. Blood pressure varies with the time of day, as might the effectiveness of treatment, and archetypes used to record the data should include the time taken.

Using Medications- 
  The goal of treatment should be in B/P control of <140/90 mmHg for a significant amount of patients, and lower in certain contexts such as diabetes or kidney etiology (some textbooks recommend keeping levels below 120/80 mmHg).30 Each added drug may reduce the systolic B/P by 5-10 mmHg. It is not uncommon to have multiple drugs prescribed to the patient in order to achieve the necessary B/P control.
  Commonly used drugs include the following typical groups:31 
ACE inhibitors such as captopril, enalapril, fosinopril (Monopril), lisinopril (Zestril), quinapril, ramipril (Altace).
Angiotensin II receptor antagonists may be used where ACE inhibitors are not tolerated e.g. telmisartan (Micardis, Pritor), irbesartan (Avapro), and losartan (Cozaar), valsartan (Diovan), and candesartan (Amias).
Calcium channel blockers such as nifedipine (Adalat), amlodipine (Norvasc), diltiazem, verapamil.
Diuretics: e.g., bendroflumethiazide, chlortalidone, hydrochlorothiazide.
Other Used Groups May Include-
Α - (α) blockers include prazosin, or terazosin.
Β- (β) blockers include atenolol, labetalol, metoprolol (Lopressor, Toprol-XL), and propranolol.
Direct renin inhibitors include aliskiren (Tekturna).
Several Agents May Be Given Simultaneously-
  A fixed combination of the angiotensin-converting enzyme, (i.e., [ACE] inhibitor), perindopril and the calcium channel blocker amlodipine, recently have been proved to be effective even in patients with additional impaired glucose tolerance and in patients with metabolic syndrome.32 Keep in mind that with ACE and/or α-blockers administration therapy, there is the possibility of a metabolic anti-reaction that can cause serious internal and external swelling in ears, mouth, and throat. In extreme conditions may cause Stevens - Johnson syndrome (SJS), (i.e., a drug eruption caused by a sensitivity or allergy to some medications). Symptoms range from a mild rash to life-threatening anaphylaxis.33,34

Awareness of Complications- 
  Primary or secondary HT is a major risk factor for all clinical manifestations of atherosclerosis since it is a risk factor for atherosclerosis in itself.35 In addition, it is an independent predisposing factor for heart failure, coronary artery disease (CAD), stroke, renal disease, and peripheral arterial disease (PAD). It is the most important risk factor for cardiovascular morbidity and mortality, within an industrialized nation.36 

Epidemiology Findings- 
  Near the beginning of the twenty-first century, it was estimated that HT worldwide affected nearly one billion people, and the findings are predicted to increase to 1.5 billion by 2025.37 In addition, medical analysts have estimated that over 43 million people in the United States have HT or are taking an anti-hypertensive medication, which is almost 24% of the adult population.38 
  This proportion changes with race, being higher in African-Americans and lower in Caucasians including Mexican- Americans. Second, it will change with age, because in industrialized countries systolic B/P rises throughout life, whereas diastolic BP rises until age 55 to 60 years and thus a greater increase in prevalence of HTN among the elderly. Also, in geographic patterns, because HTN is more prevalent in the southeastern United States, and gender becomes an important factor as once taught men were at higher risk. Finally, you have to take into account the socioeconomic status, which is an indicator of one’s lifestyle.
  The World Hypertension League (WHL), an umbrella organization of 85 national hypertension societies and leagues, recognized that more than 50% of the HTN populations worldwide are unaware of their condition.39

  The primary care nurse owes it to themselves and their patients to be informed on the chronic diseases they manage in order to achieve maximum patient compliance and satisfaction. Also, remember that HTN by its self is a reversible condition, not a disease. Well informed, confident practitioners will be able to deliver evidence-based structured advice, and in doing so reduce morbidity and mortality rates from cerebrovascular accidents and cardiovascular disease for patients regardless of age, gender, or ethnicity. In addition, HTN and its management is not a one-size-fits-all approach.

The professional health care practitioner should also explain the diagnostic procedures such as blood studies, computed tomography scan, and magnetic resonance imaging to the patient and make him and/or her feel less frighten.
  Finally, explain with sensitivity and with a concerned heart the underlying disorder and treatment plan. You are the extension of human-science with the compassion for caring. Let your patients feel alive and well because you bring them hope.


  1. Dr’s Chin, KM, Rubin, LJ (Jan.2008).  Journal of the American College of Cardiology, Pulmonary Arterial Hypertension 51:  1527-1538, doi: 10.1016/j.jacc 2008.01.024.

  2. American Heart Association, Circulation (2004).  “Definition of Metabolic Syndrome” 109:  433-438. Cir. 0000111245.

  3. Oparil S, Zaman MA, Calhoun DA (November 2003).  “Pathogenesis of hypertension”. Ann. Intern. Med. 139 (9): 761-76. PMID 14597461.

  4. Chobanian AV, Bakris GL, Black HR, et al., (December 2003). “Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure”.  Hypertension 42(6):  1206-52. 

  5. Guyton & Hall (2005).  Textbook of Medical Physiology (7th ed.).  Elsevier-Saunders. P.220 

  6. Chobanian AV, Bakris GL, Black HR, et al., (December 2003).

  7. “Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure”. Hypertension (December 2003).  42 (6):  1206-52.  Cited recently in (2009).

  8. Nursing and Midwifery Council. Code of conduct. London:  NMC; 2007.

  9. Amer. H. Assoc. Heart Disease and Stroke Statistics (2009).  Available @ Also, see the 18th rev. ed. The Merck Manual of Diagnosis and Therapy, Whitehouse Station, NJ Merck & Co. Inc.

  10. “Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure”. Hypertension (December 2003).  42 (6):  1206-52. Chobanian AV, Bakris GL, Black HR, et al., Indorsed by the American Heart Association (2003) and the American Medical Association (2003).

  11. Papadakis, MA; McPhee, SJ. Current Medical Diagnosis and Treatment 2009. McGraw-Hill Professional. ISBN 0-07-159124-9.

  12. “Hypertension: eMedicine Pediatrics: Cardiac Disease and Critical Care Medicine”. Cited in (2009).

  13. “Hyperthyroidism: eMedicine Endocrinology”. Cited Retrieved (2009).

  14. American Medical Association, Complete Medical Encyclopedia (2008 Rev. ed). Random House Reference: New York.

  15. “Hyperthyroidism: eMedicine Endocrinology”. Cited (2009).

  16. Goldberg, GD Paper on “Electrophysiology and Electrocardiography Review” (2008).  Submitted to the AMA board review and orientation for fellows and interns. 

  17. Dr’s. Curry, CL. Robinson, H. Brown, J. Olivan, M  Sami, M.  Honos, G Howard Univ. USA, Hospital Clinico de Sevilla, Sevilla, Spain, Royal Victoria Hospital, Montréal, Québec, Canada. Am. J. Hypertens. (1996) 9, 828-832; revised and cited 9n (Sep. 2009) as a reprint. 

  18. “Hyperthyroidism:  eMedicine Endocrinology”. (2009).

  19. J. Am. Coll. Cardiol, (Jan. 2008).  By the American College of Cardiology Foundation, 51: 1527-1538.

  20. Aminoff UB, Kjellgren K, The Nurse – a resource in hypertension care.  Jurnal of Adv. Nursing, 2001; 35:582-589.

  21. World Health Organization.  Pocket guideline with WHO/ISH Cardiovascular Risk Prediction Charts for WHO epidemiological sub-regions EUR a, (2007).  Cited in, Hypertension 2005; 46:66-70.

  22. AMA, Complete Medical Encyclopedia (2008 ed.).  Random House Reference: New York

  23. “Hypertension and Pregnancy:  eMedicine Obstetrics and Gynecology”.  Visit web site (2009).

  24. Kosugi T, Nakagawa T (Feb.2009) Journal of Human Hypertension 23 (2):  75-76

  25. Dickson ME, Sigmund CD (July 2006) “Genetic basis of hypertension:  revisiting angiotensinogen”. Hypertension, 48 (1):  14-20. 

  26. AMA, Complete Medical Encyclopedia (2008 ed.).  Random House Reference Publishing:  New York

  27. Dr’s Alice V, Stanton, Patrick Dicker, Eoin T. O’Brien, Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, Dublin, Ireland.  American Journal of Hypertension 2009; 22, 9, 954-957. 

  28. McGrath, B (1996).  “Is white-coat hypertension innocent?”  Lancet 348 (9028):  630.

  29. American Heart Association, “Monitoring of High Blood Pressure”

  30. “Pre-hypertension:  Early-stage High Blood Pressure,” (July 2009).  WebMD. 

  31. “Hypertension-quick reference guide”.  National Institute for Health and Clinical Excellence, (June 2006).

  32. Widimsky, J (Feb. 2009).  “The combination of an ACE inhibitor and a calcium channel blocker is an optimal combination for the treatment of hypertension”. Hypertension 55 (2): 123-130. 

  33. AMA, Complete Medical Encyclopedia (2008 ed). Random House Reference Publishing:  New York. 

  34. R. Patterson, MS Dykewicz, A. Gonzalzles, D. Green (1990).  Chest, vol. 98, cited in (2009) Chest, Erythemia mutiforme and Stevens-Johnson syndrome, descriptive and therapeutic controversy. September 39: 545-548.

  35. Insull W (Jan. 2009).  “The pathology of atherosclerosis:  plaque development and plaque responses to medical treatment”.  The American Journal of Medicine 122 (I Suppl): S3-S14. 10.013.

  36. Novo S, Lunetta, M (Jan. 2009).  “Role of ARB’s in the blood hypertension therapy and prevention of cardiovascular events”.  Current Drug Targets 10 (1):  20-25.

  37. Kearney PM, Whelton M (2005).  “Global burden of hypertension:  analysis of worldwide data”.  Lancet 365 (9444): 217-223.

  38. Kearney PM, Whelton M (2005).  “Global burden of hypertension…” pp 63-71.

  39. Chockalingam A (May 2008).  “World Hypertension Day and global awareness”. The Canadian Journal of Cardiology 24 (6):  441-444. 

Short Bio of Dr. Gary D. Goldberg, PhD 

Over 30 years experience in the Medical field, At UCLA and Pacific Hospital of the Valley, as a Chief Technologist and Analyst, Visiting Professor and Instructor for continuing education at UCLA School of Nursing and Writer/Speaker at the School of Medicine from 1978-2008.

From 2003-2008 Dr. Goldberg has collaborated and published through Blackwell Publishing Co. (Medical Division) and Journal of Americana College of Cardiology plus 15 published abstracts with UCLA Dept. of Bio-Medical Engineering and the Dept. of Cardiology.

Current title: Clinical Professor of Medical Education with Angeles College of Nursing, in Los Angeles, Ca.

Dr. Goldberg has written two major academic course textbooks for Angele College of Nursing and has represented advanced nursing education course curriculum through the State Dept. of California and approved by the ANA for CEU(s) and the AMA CMU Level 1 Credit for physicians.

In addition, Dr. Goldberg is currently an adjunct Professor for Kaplan University, e.g., through the Washington Post Inc., South Florida. Department of Health and Science plus the Dept. of Humanities.

His wife, Cindy L. Capute, has been a registered nurse for over 17 years and has managed a 200-bed acute care facility, with over 100 professional nurses from RN’s through CNA in the Los Angeles area. She keeps her ear in-tune with up-to-date nursing data and advancements in medical education. She has co-authored with Dr. Goldberg in 2005, paper presented to the Cardiology-Electrophysiology Research Group that has changed the dynamics of elector-static reading with regards to acute atrial anomalies.

This finding allowed Dr. Goldberg, to publish the “Goldberg Protocol” for Cardiac placements in the field and under clinical supervision using a tilt-table and the 12 +3 Leads or the vector positioning for additional cardiac patient information.

To reach Dr. Gary D. Goldberg, for comments and/or professional consultation, please use e-mail address:   [email protected] 

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