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Journal of Nursing

The Signs and Symptoms’ of Cardiomyopathy: The Awareness and Actions of the Registered Nurse 

by Gary D. Goldberg, PhD Clinical Professor of Medical Education Angeles College of Nursing, Los Angeles, Ca. [email protected]


ABSTRACT


     Cardiomyopathies come from many mechanisms, but the conditions may be divided into three major types:  First, dilated or congestive.  Second, hypertrophic, and third, restrictive.  A careful history-taking by the registered nurse or practitioner along with a complete physical examination can reveal cardiomyopathies, but it is appropriate to confirm the diagnosis with a transthoracic echocardiography and selected laboratory studies. 


Key Points – 




  • Cardiomyopathies are caused by a primary disease that affects the heart muscle, and will lead to impairment from abnormal ventricular function. 

  • Abnormal ventricular function may be the result of the following:  (1) systolic dysfunction, (2) diastolic dysfunction, or (3) a combination of both.  

  • In patients with hypertrophic (i.e., enlargement or overgrowth of an organ due to an increase in size of its cells) cardiomyopathy (HCM), a dynamic outflow tract obstruction and secondary mitral regurgitation may cause symptoms of exertional dyspnea, angina, and syncope.  

  • Some cardiomyopathies are reversible.  Therefore, every effort from the physician’s team, (e.g., lead registered nurse and/or practitioner, along with the nursing education dept. and physical therapy team), should be made to identify the reversible forms and to treat them appropriately in order to prevent further deterioration.  



Background –


     The hallmark of hypertrophic cardiomyopathy is myocardial hypertrophy (e.g., the myocardium thickening of the wall size and shape), that is inappropriate and often A-symmetric that occurs in the absence of an obvious inciting hypertrophy stimulus.  Although any region of the left ventricle (LV) can be affected, hypertrophy frequently involves the interventricular septum which can result in an outflow tract obstruction.  In many clinical studies regarding the electrophysiology of hypertrophic cardiomyopathy, patients have preserved systolic function with impaired LV compliance that results in diastolic dysfunction whether or not the outflow tract obstruction is present. 1  


 Clinical Manifestations –


     The nurse- clinician should take extra steps in gathering patient and family history as in asking questions regarding some basic symptoms:  Is there a history of a productive cough and dyspnea, perhaps with wheezing.  Breathlessness limits the patient’s ability in the minor stresses of daily living.  Frequently there is a history of emergency hospital admissions because of respiratory infection, and sometimes necessitating mechanical ventilation.  In breathing oxygen (O₂),  there may be increasing somnolence or other symptoms of hypercapnia such as recurring headaches, confusion, and even vomiting which when combined with blurred optic discs (also, due to cerebral vasodilation), constitutes the “pseudo tumor cerebri” syndrome. 2ʹ3 


Note:  Hypoxia is usually present due to hypoventilation and sleep- apnea that may worsen at night.  Therefore, it may be wise to have a sleep study done to rule- out any pulmonary disease, along with labs for hemodynamics in patients with questionable obstructive pulmonary disease or episodes of peripheral edema on site. 4 


     Also, in regards to older adults, during the examination the nurse and/or clinician should look for nicotine staining of the fingers, which is a sign reflecting many years of heavy cigarette smoking.  The skin may be warm and the arterial pulse bounding in the high cardiac output state induced by hypoxia and hypercapnia.  The distention of the chest due to the airflow obstruction and the presence of rhonchi and wheezes secondary to chronic bronchitis usually make cardiac auscultation difficult.  Take notice with your cardiac stethoscope of a right-sided protodiastolic galloping sound (S₃) and a systolic murmur of the tricuspid regurgitant which may be audible. 


Note:  As a registered nurse or treating practitioner, if you are given the opportunity to be with your patient while the service of a 2-D Echo is being performed, please ask the clinician while he or she is recording in the short axis mode, to listen and investigate heart sounds, by placing your cardiac stethoscope over the apex and moving it over the chambers to hear the various sounds. This will bring alive your sense of sight and sounds to a new level. 


 Signs of enlargement of the right ventricle (RV) may be attributed to mild-to-moderate pulmonary hypertension (PHTN) that is common in severe obstructive bronchitis and emphysema.  Pulmonary artery systolic pressure is typically in the range of 50 to 60 mmHg, far below the systemic levels that may occur in patients with congenital heart disease and in those with primary pulmonary hypertension. 5  


Note:  The investigating registered nurse should be aware that patients with cor pulmonale due to “chronic obstructive lung disease” (COLD), usually have an advanced form of the disease with FEV₁ < 1.0 L and Pа₀₂ < 60 mmHg.  Also, the RV failure secondary to COLD often occurs when there is “acute-on-chronic” respiratory failure with evidence of hypoxemia.6       


Laboratory Examinations for Evidence Based -  


    The electrocardiogram (ECG) will often show sinus tachycardia (Sin tach) or atrial fibrillation (AFib), ventricular arrhythmias, and left atrial abnormalities.  Also, look for diffuse non-specific ST-T wave abnormalities and sometimes an intraventricular conduction defect (IVCD), with global low voltage criteria.  These are all electrical nodal signs of possible pre-cardiomyopathy.  Next, order a complete 2-D echocardiography and radionuclide- ventriculography, which my show left ventricular dilatation, with normal or minimally thickened or thinned walls, along with systolic dysfunction (reduced ejection fraction).   


Note:  The nurse-clinician should investigate, identify, and document, then forward these signs and symptoms to the primary physician, in order for possible further investigation into ordering a cardiac catheterization and/or coronary angiography.  In many case studies reported within the U.S. patients who pursue an inexorably down-hill course, and those who are over 55 years of age, die within 3 years of the onset of symptoms. 7


  History Taking Protocols –    


     Patients with hypertrophic cardiomyopathy (HCM) may indeed appear A-symptomatic.  The nurse and/or practitioner should be able to detect and document some of the signs and symptoms which can include dyspnea, syncope, pre-syncope, angina, palpitations, orthopnea, paroxysmal nocturnal dyspnea, dizziness, congestive heart failure, and through atopy findings, in sudden cardiac death. 


Dyspnea –




  • Dyspnea (i.e., sensation of difficult or uncomfortable breathing), appears to be one of the most common presenting symptoms that occurs in as many as 90% of symptomatic patients. 8 

  • Dyspnea is largely a consequence of elevated left ventricular (LV) diastolic filling pressures (P₀₂), and transmission of those elevated pressures back into the pulmonary circulation. 

  • The elevated LV filling P₀₂ principally results from impaired diastolic compliance as a result of marked hypertrophy of the ventricle. 9  



Syncope –   




  • Syncope (i.e., loss of consciousness caused by a temporary deficiency of blood supply to the brain), is a common symptom of HCM, resulting from inadequate cardiac output on exertion or from cardiac arrhythmia, either tachycardia or sever bradycardia. 

  • Some patients have abnormalities in sinus-node function, leading to sick sinus syndrome (SSY).  

  • Syncope is usually common within children and young adults with small LV chamber size and evidence of ventricular tachycardia on ambulatory monitoring.  

  • Syncope identifies children and younger adults with HCM, significantly increases their risk of sudden death and warrants an urgent evaluation and aggressive treatment plan.  



Pre-Syncope –




  • Also, pre-syncope refers to “graying- out” spells that occur in the erect posture and can be relieved by the individual immediately lying down.  Also, these symptoms are exacerbated by vagal stimulation.  

  • Pre-syncope may occur commonly in patients with HCM and identifies a sub-group of patients who may be at increased risk for sudden death.  



Note:  After your findings and documentation as an investigating nurse- clinician, consult with the cardiologist and/or electro-physiologist for possible specific cardiac studies which should include the non-invasive cardio-diagnostic department, to run either a Frank- vector-cardiogram or Single-Average (e.g., late potential diagnostics).   Like syncope, pre-syncopal episodes warrant a direct evaluation to rule-out (R/O) malignant arrhythmias.  A thorough investigation is warranted to also, R/O potential malignant etiology of pre-syncopal symptoms.10ʹ11


Angina -   




  • Symptoms of angina (i.e., Latin for “choking pain of the chest,” also, tightness or heaviness), have been seen in child and young adults with HCM and occur in the absence of detectable coronary atherosclerosis.  

  • Signs of impaired diastolic relaxation and markedly increased myocardial oxygen consumption due to ventricular hypertrophy result in subendocardial ischemia, particularly during exertion. 12  



Palpitations –




  • Palpitations (i.e., sensation of a fast or irregular heartbeat; also common with hypertension patients, mitral valve prolapse, hyperthyroidism, anemia, and coronary artery disease), are usually due to arrhythmia, which can be seen on an ECG monitoring device or a 48 hours of electrogram recording known as an Event Recorder (AECG). 13 

  • Some of the more common electro-arrhythmias include: premature atrial and ventricular beats (PAC’s and/or PVC’s), sinus pauses (S-P), intermittent atrioventricular block (AVB), atrial fibrillation (AFib), atrial flutter (AF), supraventricular tachycardia (SVT), and ventricular tachycardia (VT).  



Note:  All nursing-clinicians should keep in mind, that non-sustained ventricular tachycardia is another bio-marker, and is included for higher risk factors of sudden death.14  


Orthopnea and Paroxysmal Nocturnal Dyspnea -  




  • Orthopnea (i.e., difficulty breathing while lying down) also, a sign of heart failure, lung problems, or by anxiety, may be an early sign of congestive heart failure (CHF) and are observed in patients with severe cases of HCM.  

  • Also, symptoms of paroxysmal or chronic dyspnea occur when the impaired diastolic function and elevated LV filling P₀₂ result in pulmonary venous congestion.    



Dizziness -  




  • Dizziness (i.e., inability to maintain normal balance), which includes high B/P, intoxication, and medications, which may accompany a complete loss of consciousness, when other symptoms are present such as light-headedness persists for three weeks or longer. Plus, a medical examination may reveal possible neurological issues. Have the treating physician and/or clinician order a consultation with both the cardiology and neurology team.  



Note:  The nurse’s sense (awareness) of importance due to acute findings through observation and documentations may allow her and/or him to ask the treating physician (based on specific evidence through critical findings) to order an electroencephalogram (EEG) study, or a computed tomography (CT) to R/O secondary neurological problems caused by primary HCM.   




  • Dizziness also may be caused by arrhythmia-related hypotension (i.e., low B/P), and decreased cerebral perfusion. 

  • Non-sustained arrhythmias often cause symptoms of dizziness and pre-syncope, whereas sustained arrhythmias are more likely to manifest in syncope, collapse, and/or in sudden cardiac death. 15  



Congestive Heart Failure –




  • The ‘target organ’ disorder of congestive heart failure (i.e., pumping failure, pulmonary edema), begins to fail, it works harder to compensate a response that worsens the disease over time. 

  • Congestive heart failure (CHF) can occur at any age, plus in the Ac₃ stage, can result from a coronary event such as a heart attack or cardiac arrhythmia.  

  • More than 75% of patients with CHF in the U.S. are older than 65 years of age.  Also, CHF is the leading cause of hospitalization in older adults. 16  



Note:  The pathophysiology of CHF is similar in younger children, about 10% at initial presentation, most commonly in infants younger than 1 year of age.17 The systolic function in children with HCM is almost always well preserved, at least until the last stage of the disease.  Patients with CHF have a high likelihood of recurrent heart failure due to both mitral regurgitation and profound diastolic dysfunction.18  


Sudden Cardiac Death - 




  • Sudden cardiac death has the highest incidence in adolescent children but not excluding younger adults, and is typically associated with sports or vigorous exertion.  

  • The arrhythmia that causes sudden death is usually but not exclusive alone to, ventricular fibrillation. 

  • A pathophysiology and epidemiology report have shown in more than 80% of patients with HCM and with known congenital heart disease brings a higher risk for sudden cardiac death. 19 

  • For many patients with HCM develop over time, ventricular fibrillation (VFib) following atrial fibrillation (AFib), also atrial flutter (AF), and supraventricular tachycardia (SVT’s) associated with Wolff-Parkinson-White (WPW) syndrome. Commonly found in documented findings, there ventricular tachycardia (VT) with low-cardiac-output, associated with hemodynamic collapse. 20 

  • Early diagnosis is of prime importance, if death is to be prevented by prescription of an appropriate levels of safe activity, medications, surgery (e.g., electrophysiology invasive procedures), and/or an implantable cardioverter defibrillator may be in order.  

  • Remember, that because this is an autosomal (i.e., genetic disorder) dominantly inherited disease, an investigation with screening of first-degree relatives, which should include a physical examination, and an electrocardiography (ECG) screening, with a transthoracic 2D- echocardiography, with color flow mapping, which will be useful to identify additional family members with possible cardiomyopathy (CM) before the onset of significant symptoms or sudden death occur.   



Physical Examination Findings –   


    Most patients with HCM or cardiomyopathy (CM), excluding the pediatric patients with known congenital heart disease, do not have outflow tract obstruction and may show completely normal during the physical examination findings.  Therefore, it is important that the nurse investigates further, using her skills in evidence-based practice towards listening to heart sounds, cardiac impulse, murmur, and other findings: 




  • The first heart sound (S₁) is influenced by the position of the mitral leaflets at the onset of ventricular systole.  The amount of tissue, air, or fluid between the heart and the stethoscope may be louder if diastole is shortened because of tachycardia.  Also, in a prolonged P-R interval, or with an imperfect closure due to reduced valve substance in the mitral regurgitation S₁ sound may appear soft. 

  • The second heart sound will appear to sound “split”.  Splitting in S₂ that persists with expiration from the pulmonic area or left sternal border may be due to many causes, including patients with chronic pulmonary hypertension.  The oxygen partial pressure (P₀₂) may appear loud and also, patients with HCM/CM will split paradoxically. 

  • The third heard sound (S₃) is a low-pitched sound produced in the ventricle after the closing sound of the aortic valve (A₂), at the termination of rapid filling.  In younger patients with CM a sound or “gallop” may appear but does not have the same ominous significance as in patients with valvular aortic stenosis (VAS) or in older adults. 21  Place the stethoscope at the left ventricular apex during expiration and with the patient in the left lateral position. 

  • The fourth heart sound (S₄) is frequently heard in patients with HCM, and is due to atrial systole against a highly non-compliant LV wall.  It is usually loudest at the left ventricular apex, when the patient is in the left lateral position.  The right-sided (S₄) sound is present in patients with right ventricular hypertrophy, secondary to either pulmonic stenosis or pulmonary hypertension. 22 



Cardiac Impulse – 




  • The apical precordial impulse is frequently laterally displaced and is usually abnormally forceful and enlarged in patients with HCM. 

  • Double apical impulse resulting from a forceful left atrial contraction against a highly non-compliant LV and occurs in young children plus, a variance within younger adults with HCM. 23  

  • A triple apical impulse are rarely but does accrue from a belated systolic bulge (e.g., sudden increase sound) that appears when the heart is almost empty and is performing near-isometric contraction. 24ʹ25 



Murmurs -   




  • Systolic ejection murmurs are often “crescendo-decrescendo” in shape when blood is ejected across the aortic or pulmonic outflow tracts. 26 Place your stethoscope between the apex and the left sternal border; it radiates to the suprasternal notch but not to the carotid arteries or neck.  The murmur may vary with the subaortic gradient across the LV outflow tract. 

  • The systolic or holosystolic (pansystolic) murmurs are generated when there is flow between two chambers that have widely different pressures throughout systole.  The holosystolic murmur of the mitral regurgitation is heard at the apex and left axilla in patients with systolic anterior motion of the mitral valve and significant LV outflow tract. 27

  • Note:  In patients with congenital heart defects or in HCM there may appear a continuous murmur sound.  This begins in systole, peak near S₂, and continues into all or part of diastole.  This continuous flow is due to a communication between high-and low-pressure areas that persists through the end of systole and the beginning of diastole. 


  •  




Restrictive Cardiomyopathy - 

          The hallmark of the restrictive cardiomyopathies is abnormal diastolic function; while the ventricular walls are excessively rigid and impede ventricular filing.  Also, myocardial fibrosis, hypertrophy, or infiltration due to a variety of causes is usually responsible.  The cardiologist and/or electro physiologist can determine through a series of diagnostic exams which may include the specific roentgen (chest x-rays), nuclear imaging, and a transesophageal -echocardiogram. 


Note:  The Transesophageal-Echocardiogram (ETT) procedure allows the cardiologist to view the heart while it is moving and to observe its main pumping chambers, along with the shape and thickness of the chamber walls as well.  Through this unique procedure, it is also possible to determine the volume and direction of the blood flow cycle in the heart.  This assessment is especially important for the HCM patient to determine size, pumping strength, abnormal blood flow patterns, and structural abnormalities. 


          The myocardial involvement with the protein “amyloid,” once deposited in the heart muscle, kidneys, or nervous system, it cannot be broken-down, nor recycled by the body and will lead to amyloidosis.  The signs and/or symptoms that you may be observing will include: swollen legs and ankles, weakness, weight loss, shortness of breath, dizziness, diarrhea, severe fatigue, enlarge tongue, and numbness in the extremities.   Also, this is a common cause of secondary restrictive cardiomyopathy. 28


     In many of these conditions, particularly those with substantial concomitant endocardial involvement, partial obliteration of the ventricular cavity by fibrous tissue and thrombus contributes to the abnormally increased resistance to the ventricular filling.  Thromboembolic complications have been reported in the U.S. in about a third of these patients. 29    


Conclusion –   


     HCM may be characterized morphologically and defined by a hypertrophied, non-dilated LV in the absence of another systemic or cardiac disease that is capable of producing an abnormal wall thickening evident (e.g., systemic hypertension and/or valvular stenosis). Indeed, clinical diagnosis for the most part and cost saving measures remain today through an electrocardiograph (12-lead ECG) or an event recorder (AECG).  Plus a transthoracic 2-dimensional echocardiograph, and with a cardiac magnetic resonance imaging, by detection of otherwise unexplained abnormal LV function.  Also including evidenced-based suspicion that may be raised after clinical profiling and family screening is gathered.   


     Medical research institution across the world has open new pathways into genetic encoding, and ion channelopathies, both nocturnal and sudden unexplained death syndromes in pediatric and older adults, are investigated through mutations in defective ionic channel proteins and ion channel electrical disorders which include the LQTS, and/or short-QT syndrome.  Also notable, are the SQTS syndrome, and the Brugada syndrome which includes gene encoding.  These electro-physiological findings are making there way into the care of the trauma physician teams within North American and Southeast Asia. 


     Throughout this article, the author’s have strived to bring a useful  guideline towards the registered nurses and/or nursing practitioners, in order to enhance and encourage advance critical-thinking that she and/or he may act upon within a medical institution, outpatient walk-in clinic, or emergency room department. 


     Also, the authors would like to give their thanks to both learning institutions (Angeles College of Nursing and the advanced Continuing Nursing Education Department at Kaiser Permanente Health-Care Facilities for the advancement of applied nursing education and information.  Also, the physicians (e.g., interns, 3rd year residence, and fellows), who are finishing their cardiology and electrophysiology services.  



[1] Jarcho, J.A., McKenna, W., Pare, J.A., et al.  Mapping a gene for familial hypertrophic cardiomyopathy to chromosome 14q1. N Engl J Med. Nov. 16, 1998; 321 (20): 1372-8.


[2] Incalzi, R.A., et al:  Electrocardiographic signs of cor pulmonale:  A negative prognostic finding in chronic obstructive pulmonary disease.  Circulation 99: 1600, 1999. 


[3] Weitzenblum, E., et al:  Benefit from long-term O₂ therapy in chronic obstructive pulmonary disease patients.  Respiration. 59 (Suppl. I): 14, 1994.


[4] Haraldsson, A.  et al:  Comparison of inhaled nitric oxide and inhaled aerosolized pros-tacylin in the evaluation of heart transplant candidates with elevated pulmonary vascular resistance.  Chest 114:780, 1998.


[5] MacNee, W., Pathophysiology of cor pulmonale in chronic obstructive pulmonary disease.  Amer Respir Crit Care Med. 150:833, 1994.


[6] Rich, S:  Cor pulmonale, inHeart Disease, 6th edE. Braunwald (ed). Philadelphia, Saunders, 2001.


[7] Dec, GW, Fuster, V:  Medical progress:  Idiopathic dilated cardiomyopathy.  N Engl J Med (1994). 331: 1564,


[8] Colan, S.D., Lipshultz, S.E., Lowe, A.M., et al.  Epidemiology and cause-specific outcome of hypertrophic cardiomyopathy in children: findings from the Pediatric Cardiomyopathy Registry.  Circulation. Feb. 13, 2007; 115(6): 773-81.


[9] Braunwald, E., (Sir. Ed).  et al.  5th edHeart Disease:  A Textbook of Cardiovascular Medicine.  Vol. 1, 1997 edition.  Symptoms of Heart Failure, Respiratory Distress:  Dyspnea. Philadelphia:  W.B. Saunders Co. pp. 439-43. 


[10] Perloff, J.K., Middlekauff, H., Child, J.C., Goldberg, G.D., et al.  Electrophysiologic Properties of the Atrialized Right Ventricle in Ebstein’s Anomaly. Published through the Ahmanson/UCLA Adult Congenital Heart Center and the Dept. of Pathology Laboratory of Medicine, and the David Geffen School of Medicine at UCLA, Los Angeles, Cal. Spring, 2005. Also, cited in Elsevier:  Amer J Card (2005): Issue 12, under Science Direct Abstract. 


[11] Perloff MD, J.K., Middlekauf MD, H.R., Child MD, J.S., Stevenson MD, W.G., Miner NP, P.D., Goldberg PhD, G.D., Usefulness of Post-Ventriculotomy Signal Averaged Electrocardiograms in Congenital Heart Disease.  Amer J Card. (2006): Vol. 98, Dec. Issue 12, pp. 1646-1651. @ www.ajconline.org/article/S0002-9149(06)01726-7 abstract.


[12] ________, et al Amer H Assoc. Science Advisory & Coordinating Committee on Feb. 1, 2006. Published findings on: Cardiomyopathy, Hypertrophic in Adolescents and Young Adults. © No. 71-0358. http://www.ahajournals.org/cgi/content/full article. 


[13] Crawford, M.H., Chair, Bernstein, S.J., Committee Member, et al.  ACC/AHA Practice Guidelines.  J Amer Coll Card. Vol. 34, Issue 3, Sept. © 1999 American College of Cardiology Published by Elsevier Science Inc.  ACC/AHA guidelines for ambulatory electrocardiography… 1999, pp. 912-948.   


[14] Maron, B.J., Roberts, W.C., Epstein, S.E. Sudden death in hypertrophic cardiomyopathy:  a profile of 78 patients.  Circulation. Jun 1982: 65(7): 1388-94. Lippincott Williams & Wilkins Publishes the AHA Journals for the Amer H Assoc cited in: http://circ.ahajournals.org/


[15] Wolf, C.M., Moskowitz, I.P., Arno, S, et al.  Somatic events modify hypertrophic cardiomyopathy pathology and link hypertrophy to arrhythmia.  Proc Natl Acad Sci U S A.  Dec. 13, 2005: 102(50):18123-8.  


[16] Rich, M.W. et al.  The Geriatric Cardiology Section:  Barnes-Jewish Hospital, Washington Univ. Med. Center:  St. Louis, Mo.  USA. The EpidemiologyPathophysiology, and Etiology of Congestive Heart Failure.  J Amer Geriatr Soc. 1999, Apr. 46(4): 536-9.


[17] Morita, H, Rehm, H.L., Menesses, A. et al.  Shared Genetic Causes of Cardiac Hypertrophy in Children and Adults.  N Engl J Med.  May 1, 2008; 358(18): 1899-908. http:/www.nejm.org// The New England Journal of Medicine is owned, published, and copyrighted © 2009 Massachusetts Medical Society


[18] Spevack, D.M., Hypertrophic Cardiomyopathy and the Outflow Tract Obstruction.  N Engl J Med.  May 1, 2003; 348(18): 1815-6. http:/ www.nejm.org// The New England Journal of Medicine is owned, published, and copyrighted © 2009 Massachusetts Medical Society.


[19] Ostman-Smith, I., Wettrell, G., Keeton, B., et al.  Echocardiographic and electrocardiographic identification of those children and young adults with hypertrophic cardiomyopathy who should be considered at high-risk of dying suddenly.  Cardiol Young.  Dec. 2005; 15(6): 632-42. 


[20] Ostman-Smith, I., Wettrell, G., Keeton, B. et al.  Cited inCardio Young. Dec. 2005; 15(6): 632-42. 


[21] __________:  Physical examination of the heart and circulation; inHeart Disease, 6th edition. E. Braunwald et al. (Eds).  Philadelphia:  Saunders, 2001.


[22] Braunwald, E: The clinical examination; in: Primary Cardiology.  L. Goldman, E. Braunwald (Eds).  Philadelphia: Saunders, 1998, pp. 27-43.


[23] Perloff, J.K (Ed):  Physical Examination of the Heart and Circulation2nd ed.  Philadelphia: Saunders, 1990.


[24] Perloff, J.K (Ed): Physical Examination of the Heart and Circulation.


[25] Epstein, A.E, DiMarco, J.P, Ellenbogen, K.A, et al.  ACC/AHA/HRS (2008).  Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology and American Heart Association Task Force on Practice Guidelines.  J Amer Coll Cardiol. May 27, 2008; 51(21): e1-62.


[26] Lembo, N.J. et al.  Bedside Diagnosis of Systolic Murmur.  N Eng J Med318:1572, 1998


[27] __________: Physical examination of the heart and circulation, in Heart Disease, 6th ed. E. Braunwald et al. (Eds).  Philadelphia:  Saunders, 2001.


[28] Braunwald, E: The clinical examination, in Primary Cardiology.  L. Goldman, E. Braunwald (Eds). Cardiomyopathies: sec. 238: Philadelphia: Saunders, 1998.


[29] Mason, J.W. Classification of cardiomyopathies.  In:  Fuster, V., Alexander, R.W, O’Rourke, R.A., (Eds).  Hurst’s the Heart, Arteries and Veins.  10th ed. New York: NY.  McGraw Hill; 2001: 1941-46. 


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 1995-2008.


From 2003-2008 Dr. Goldberg has collaborated and published through Blackwell Publishing Co. (Medical Division), and Journal of American College of Cardiology plus 15, published abstracts through UCLA Dept. of Internal Medicine 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.


His wife, Cindy L. Capute-Goldberg, 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 has co-authored with Dr. Goldberg in 2005, a manuscript presented to the Cardiology-Electrophysiology Research Group (i.e., DMPG), that has changed the dynamics of electro-static reading with regards to acute atrial anomalies. 


This finding allowed the author to publish the ‘Goldberg Protocol’  for Cardiac placements in the field and under the Dept. of Medicine Chair, in using a tilt-table with the 12 +3 Leads or the vector positioning for additional cardiac patient information.


To reach Dr. Gary D. Goldberg, for comments and/or consultation, please use e-mail address:  [email protected]   or cell phone contact:  818-610-9017.







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