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Journal of Nursing

Basic Cardiac Assessments: Physical Examination, Electrocardiography, and Chest Radiography 

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


ABSTRACT


The human heart is one of the major organs adversely affected by high blood pressure.  Therefore, the registered nurse must provide a careful and thorough evaluation of the assessments needed via the cardiac structure and function (i.e., including visual signs, all non-and invasive cardiac medical devices), which is an obligatory part of the examination of the hypertensive patient.  


Key Points – 



  • Hypertensive heart disease can be detected by a clinical examination, ECG, and other cardiac imaging devices.

  • Left ventricular hypertrophy (i.e., LVH), may be a manifestation of ‘target organ damage’ and may imply an adverse prognosis from an internal medicine physician or a cardiology clinician for aggressive therapy in the hypertensive patient. 

  • The level of systolic and diastolic blood pressure are directly related to coronary artery disease symptoms, both morbidity and mortality.

  • The ECG/EKG monitoring system today still remains the “gold standard” method for detecting LVH despite its relative lack of sensitivity. 


Performing the Physical Examination – 


     The persistent and presence of abnormalities on the cardiac and vascular physical examination, preformed by the cardiac nurse or clinician may contribute significantly to the cardiac assessment of the hypertensive patient and to cardiovascular risk stratification as recommended by the Council on High Blood Pressure Research. 1 The presences of ‘target organ’ damage or clinical cardiovascular disease (e.g., the detection of left ventricular hypertrophy LVH or peripheral vascular disease PVD), may prompt a more aggressive antihypertensive therapy and risk factor modification program for the patient.   


     The most direct association of hypertension (i.e., HTN), with acute (i.e., Ac₃), and chronic coronary syndromes is enhancement or acceleration of the atherosclerotic process in the epicardial coronary vessels.  Add in the contribution of elevated B/P to this formation, progression, and rupture of atherosclerotic plaque is of a major importance.  Within the hypertensive patient, however another mechanism is also at work.  The incidence of a possible silent myocardial ischemic episode is ever present.  As a nurse specialist, you may be working close with the electro physiologist or cardiologist team and key into another important factor, which is in the increased incidence of myocardial ischemia which may result from a supply-demand imbalance within the metabolic demands of the hypertrophied ventricle exceed coronary blood flow.  Therefore, in such an instance, myocardial ischemia or coronary insufficiency may not directly relate to the atherosclerotic process.  Because atherosclerosis is indeed a diffuse process (i.e., disseminate; to spread out), that involves the entire arterial circulation system.  Also, it is possible that atherosclerosis may be a fundamental pathogenetic contributor to the development or maintenance of HTN or other syndromes of excess vaso-reactivity. 2


Risk Factors –


     As part of your assessment strategies, ask your patient if he and/or she has or have had an episode of angina pectoris.  A diffuse pain or discomfort in the chest, which is often described as a tightness or heaviness.  Angina itself is not a disease, but a symptom of heart disease.  Patients experience angina in different ways, but in a given individual the pattern is usually consistent.  The pain is often described as dull rather than sharp, and it typically occurs over a wide area rather than a sharply defined point.  Ask your patient to describe the location of the pain; many people place the whole hand or a clenched fist over the chest instead of pointing to a specific spot. 


Variant or Prinzmetal angina is also distinguished by attacks that occur when the patient is at rest.  This type of angina is not caused by fatty deposits in the coronary arteries, but by spasm of the arteries.  Variant angina is often accompanied by abnormal heart rhythms, such as ventricular fibrillation or ventricular tachycardia, which may increase the risk of sudden death in patients. 34 


     Atherogenesis (i.e., gruel-like, soft and pasty materials),  begins early in life, progresses slowly over several decades, and ultimately results in the development of mature atherosclerotic plaques at lesion-prone sites, as bifurcation points and areas of increased wall stress.  In the hypertensive patient, this may indeed accelerate the atherosclerotic process, through increased transmural (i.e., through any given wall, as of the body), pressure. 5 Also, the augmentation of mechanical stress, and the greater wall tension in the coronary vessel. 


     For the registered nurse, she or he clinically knows that unstable angina (e.g., burning, heaviness, aching, strangling, or compression), represents the last opportunity to restore adequate blood flow to the at-risk region of the myocardium (MV₀₂).  Assessing the breathing at rest with chest pain may be cause by Tietze’s syndrome (i.e., swelling near the rib cage, 3rd rib area), also, visual redness may be identified.


 As seen on the ECG strip or the monitoring system, the ST-segment elevation will be makeable.  Also, an echocardiographic (diminished or an absent regional wall motion), and a nuclear imaging will also show abnormalities and offer guides to therapeutic intervention. 


     In the serial ECG/EKG study, there may be an acute ST-T wave changes and also, an increase in blood levels of cardiac muscle enzymes (e.g., creatine kinase MB fraction or troponin).  In many clinical case studies, the “non-Q-wave” infarction may occur.  Therefore, a loss of subendocardial muscle mass with some preservation of the outer layers of myocytes will be noted.  The presence of the Q-wave (e.g., in lateral leads V⁵ and V⁶), may indicate a wider transmural area of injury; with patchy or incomplete loss of myofibrils (e.g., atrophy of the muscular tissue). 


Note:  Usually the development of the Q-wave generally indicates an irreversible loss of myofibrils as part of a “complete infarction”.        


Heart Sounds –


     For the registered nurse and for that matter all nurses including specialist and practitioners, one of the most valuable and useful tools must be your stethoscope (cardiac preferred).  In your assessment practice you need to know how to listen to heart sounds.  For example:  Aloud first heart sound (S₁) and brisk carotid upstroke in a hypertensive patient suggest a hyperdynamic circulatory state.  The second heard sound (S₂) is usually narrowly split, and the aortic component may be accentuated.  Although paradoxical splitting (i.e., inconsistent) of (S₂) may occur, it is uncommon and in the absence of a left bundle-branch block (i.e., LBBB), suggests left ventricular (i.e., LV), systolic dysfunction.  A third heard sound (S₃) unusual except when LV systolic failure occurs.  In almost all patients, a fourth heart sound (S₄) will develop before the (S₃) is heard, and when the (S₃) is heard, the (S₄) is almost always present. 6  


     In hypertensive patients the incidence of an (S₄) has been estimated to be between 50% and 70% especially in the presence of LVH and in older patients.  An (S₄) is the auscultatory counterpart of a vigorous atrial contraction into a relatively non-compliant left ventricle. 7  An (S₄) sound may be associated with a palpable presystolic impulse or an A (α)-wave; the (S₄) best appreciated when the patient is in the left lateral decubitus position and with the bell of your stethoscope, gently place directly on the point of maximal apical impulse for optimal sounds.  Also, you may hear an aortic systolic ejection sound (or click or clicking sound) which is occasionally heard in HTN patients and may appear to be related in a forceful expansion of the dilated aortic root. 8  In this matter, if you do hear a clicking sound, call for a cardiac clinician to confirm and possibly order a 2-D, and/or 3-D Echocardiography with color flow Doppler reading.


Electrocardiography -


     For many hospitals systems and health care facilities in the U.S. today RN’s and LVN’s/LPN’s even some NP’s are augmenting their technical skills as an ECG/EKG assessment nurse.  This means they are trained and capable to run the technical mechanism and in many instances give the treating physician a preliminary report. 


For the hypertensive patient, various ECG/EKG diagnotic criteria exist (e.g., the scoring or identifying system recommended by Romhilt- Estes score the criteria of Dr. McPhie), sum of tallest precordial R and S waves > 45 mm). 9ʹ10 In a 12 lead ECG recording, evidence of ‘left atrial abnormality’ may occur in the early stages of HTN, and may be associated with LV diastolic dysfunction which could precede abnormalities in the QRS complex. 


          Regard to the QRS amplitude, makeable overlapping exists in normal and hypertensive patients.  Factors such as age, sex, race, and body mass affect the QRS amplitude and may influence the predictive value of the QRS criteria for the diagnosis of LVH.  The ECG/EKG diagnosis of LVH is considerably strengthened in the presence of increased QRS voltages combined with typical repolarization abnormalities (e.g., LV strain pattern). 


     The QRS duration has been documented to widen with increasing severity of hypertension, and the finding of ventricular conduction delay. 11 Also, apparent on the ECG/EKG has been correlated with certain histological abnormalities (e.g., myocardial fibrosis or targeted scar tissue).  In some cases the ECG abnormalities may improve or even revert back to normal with successful anti-hypertensive therapy (decreased QRS voltage and resolution of the ST-T- wave abnormalities). 12


     Patients with hypertensive heart disease will typically show signs of LVH and almost always are seen on the ECG recording.  Therefore, when a patient presents with heart failure that is attributed to HTN and other target organ involvement,  he and/or she almost always will have some evidence of LVH on their ECG strip; if not, then other causes for heart failure must be considered. 


Importance of Hyperkalemia –


     The trained technical eye of a nurse and/or nurse practitioner can see an acute (Ac₃) hyperkalemia as it appears on an ECG/EKG recording in peaked T-waves with a narrow base.  The diagnosis of hyperkalemia is almost certain when the duration of the base is 0.20 mm or less (with a rate between 60 and 110 beats per minute). 13 As the degree of hyperkalemia increases (K₊ or potassium intoxication), the QRS complex widens, and the electrical axis usually being deviated abnormally to the left and only rarely to the right.  In addition, notice the PR interval prolongation, and the P-wave flattening until it disappears.  If this condition is not detected and assessed by the clinician (RN and/or Physician), and treated in a timely matter, death will ensue either due to “ventricular standstill “or “coarse”, slow ventricular fibrillation.14  Patient death can also result if the widening QRS complexes occurring at a fast rate are diagnosed as ventricular tachycardia and the patient is not treated with anti-arrhythmic drugs. 


Importance of Hypokalemia -


     Again, in the trained eye of the professional treating clinician, on an ECG recording the abnormality and delayed repolarization that occurs in hypokalemia is best expressed as Q-U- wave rather than through the QT prolongation.  At times on an ECG you will see notching of the T-wave and T- U-wave fusion. 15  As the serum potassium level falls, the ST segment becomes progressively more depressed and there may be a gradual blending of the T-wave into what appears to be a tall U-wave. 


     Note:  An ECG pattern similar to that of hypokalemia can be produced by some anti-arrhythmic meds, especially quinidine.  Also you should be aware when repolarization is greatly prolonged, ventricular arrhymias, including torsades de pointes (i.e., twisting of the points, a form of ventricular tachycardia nearly always due to medications over-load).  The QRS complexes tend to show a series of complexes, points up followed by complexes, points down.   


24-Hour Ambulatory ECG Holter Monitoring –


     In many academic teaching hospitals and cardiac clinics across the U.S. specially trained registered nurses and nurse practitioner are scanning the results and sending the preliminary reports to the requesting and treating physicians.  It is very important for the clinical investigations using this 24-hour ambulatory ECG monitoring device to be aware of the electrical pathophysiology signs during the scanning period.  In the hypertensive patient it has been shown a greater incidence of ventricular arrhythmias combined with LVH criteria.16   Ventricular arrhythmias appear to worsen as the hypertrophy (i.e., an increase in size of the heart muscle or any  organ), progresses. 


     Note: For many patients with the added risk factors of HTN + VEN. ARRHYMIAS + HYP. = an increased risk of sudden cardiac death syndrome.  Atrial fibrillation and other supraventricular tachycardias are more common now in patients with hypertension than in the general population findings.17 


     As for the general population, that has not been pre-diagnosed for ‘essential hypertension’  the 24-hour ambulatory ECG Holter monitoring device can prove useful in assessing atrial and ventricular arrhythmias in patients with palpitations, near syncope, or syncope episodes.


Chest Radiograph Applications –


     For the registered nurse who is working in the emergency department or on an acute surgical unit (CCU’s ICU’s, or MICU’s), she and/or he may be the first to review the radiography or fluoroscopy preliminary findings.  Also, it is becoming more prevalent among teaching hospitals today to have a few key nurses round with the treating physicians and /or team specialists. 


     Therefore, it is important for the lead nurses to have a basic and working understanding in the anatomy and physiology of the ‘target organ’ within the event horizon. One may not rely just on the routine chest radiograph to diagnose LVH alone.  Subtle dilation of the ascending aortic shadow can be found in many patients with HTN and have no apparent evidence of cardiac disease.   Sometimes in older adults and in pediatric patients (e.g., usually congenial heart disease is present), the presence of aortic coarctation as a cause of HTN can be suspected on the chest radiograph. 


Heart Dimension: Does Size Matter –


     An enlarged heart is always abnormal and identifiable within a chest x-ray or on a fluoroscopy exam.  However, mild cardiomegaly (i.e., enlargement of the heart muscle), may reflect a higher-than-average cardiac output from a normal heart, as seen in athletes.  The cardiothoracic ratio remains the simplest yardstick for assessment of the cardiac size; the mean ratio in upright postero-anterior (PA) view is 44 percent. 18 


     The nature of cardiomegaly can indeed usually be determined by the specific roentgen or chest x-ray (i.e., Wilhelm K. physicist, discovered x-ray in 1895), appearance.  As a rule, when the pulmonary blood flow (PBF) pattern remains normal, volume overload tends to present a greater degree of cardiomegaly than lesions (i.e., a pathologic change in the tissues or types of primary, secondary, and vascular lesions), with pressure overload alone. 19  For example, patients with aortic stenosis (AS) typically show features of LVH without dilatation.  On the other hand, the LV both dilates and hypertrophies in the case of aortic regurgitation (AG), which may produce a lager heart even before the development of heart failure appears.  


Assessment of Cardiovascular Dynamics –


     The chest x-ray that is taken at random largely records the diastolic image of the heart.  Fluoroscopy, on the other hand, provides a continuous vision of the pulsating organ throughout the entire cardiac cycle.  Once familiar with the normal cardiovascular movements, the fluoroscopist will find any deviation from the norm to be obvious. 20 


     Note:  On an x-ray, signs of cardiac lesions may manifest themselves usually in the ventricular systole.  Therefore, what may be missed on the x-ray film is often readily seen and diagnosed under the fluoroscope. For instance, left ventricul enlargement may be the only radiographic abnormality of severe aortic regurgitation (AR) in children or young adults.  On the fluoroscopy, the aorta will usually appear vigorously expanding in systole and rapidly collapsing in diastole.21  This dynamic alternation is characteristic of aortic regurgitation. 


Clinical Assessments – 


     As a nurse clinician, you should have a strong association between B/P elevation and other coronary risk as seen before the development of established HTN.  Compared with normotensive individuals, patients with permanent or even with “white-coat-syndrome” borderline HTN tend to be overweight; and have high cholesterol, triglycerides, plasma insulin, and hematocrit levels; and show significantly decreased HDL cholesterol levels.   Therefore, you may want to take charge, and mandate to incorporate these parameters in your evaluation of borderline HTN testing for cardiovascular risk factors. 


Note:  As part of your total assessment practice, have a plasma lipid panel ran to be determined routinely in everyone, and fasting plasma insulin values will be useful to gauge the effectiveness of non-pharmacological intervention.  Also, you should have a copy of the PDR Nurse’s Drug Handbook for quick referencing guidelines. Consider this part of your assessment gear just as your stethoscope is used for B/P and heart sound investigations.


     Also, regardless of which method or technique you choose to measure your patient’s B/P, “notations”, “notations”, and “notations” should be made of the conditions so that others can compare the findings or interpret them properly.  This is particularly critical in scientific reports, and patient nursing assessment annals.  Ultimately, the treating physician or a patient’s perception of cardiovascular risk and consequently, the quality plus the duration of life of many patients rely on the correct assessment skills of B/P and lipid panels, not only in the medical environment but also at home and/or under ambulatory care conditions.


Conclusion – 


     For the registered nurse who is working with idiopathic and/or “essential “acute secondary “target organ” disease patients, or just simply running a routine annual complete physical examination, your primary assessment skills along with any visual and articulation feed-back will become the most relevant and in many cases, the “trigger point” that will set forth in motion the investigation from both the primary clinician and the treating physician. 


     Therefore, upon opening the door and greeting your patient, your eyes, ears, and hands will become receptors within the examination which should be oriented toward clues for secondary causes of HTN, such as decreased femoral pulses, abdominal bruits, and cushingoid  stigmata (i.e., signs and symptoms of Cushing disease or syndrome: moon facies, obesity, striations, diabetes, and osteoporosis).  


     Guidelines should not be applied as a “cookbook” approach, but used as tools to assist in decision making for individualized patient care, as well as ensuring that the appropriate structures and supports are in place to provide the best possible plain of action. 


   Critical care nursing over the last decade has bridged the gap between hard-science within the scope of critical-skill-thinking and utilized correct technical skills in practice from advanced computerized medical devices that can detect abnormalities within the hypertensive patient also, promote assessment, development, and treatment plans.  


1. Izzo, J.L. Jr., MD, Black, Henry R., MD, et al.  Amer. H. Assoc. Hypertension Primer, 1st ed.   Essentials of High Blood Pressure Basic Science, Population Science, and Clinical Management.  Lippincott Wms. & Wilkins Baltimore, MA.  Chapter 109, 1999.
2. Fuster V. Lewis A. Conner Memorial Lecture:  Mechanisms leading to myocardial infarction: insights from studies of vascular biology {published erratum appears in: Circulation. 1995; 256} Circulation, 1995 90: 2126-2146.
3. Leikin, J.B., MD  Lipsky, M.S., MD Medical main editors.   American Medical Association (AMA), Complete Medical Encyclopedia.  2003 ed.  Random House Reference:  New York.
4. Solomon, A.J, Gersh, B.J.  Management of chronic stable angina: medical therapy, percutaneous transluminal coronary angioplasty, and coronary artery bypass graft surgery:  lessons from the randomized trials. Ann. Intern. Med. (1999); 128:216-223. 
5. Mac Mahon, S., Peto, R., Cutler, J., Collins, R., et al. Blood pressure, stroke, and coronary heart disease, I:  prolonged differences in blood pressure:  prospective observational studies corrected for the regression dilution bias.  Lancet.  1990; 335:765-774. Reprinted in: Circulation.  2000; 89: 2015-2010.
6. Murphy, J.G., MD, and Lloyd, M.A., MD. et al.  Mayo Clinic Cardiology, Concise Textbook 3rd ed. Mayo Clinic Scientific Press 2007. Coronary Artery Disease Risk Factors, (55): 695-715.
7. Mc Lenachan,  J.M.,  Henderson, E.,  Morris, K.I.  Ventricular arrhythmias in patients with hypertensive left ventricular hypertrophy.  N. Engl. J. Med. 1987; 317: 787-792. Reprint in N. Engl. J. Med. (2005). back issue online @www.nejm.org.// The New England Journal of Medicine is owned, published, and copyrighted © 2009 Massachusetts Medical Society
8. Levy, D., Garrison, R.J., Savage, D.D., Kennel, W.B. Castelli, W.P. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham Heart Study.   N. Engl. J. Med. 1990; 322: 1561-1566. Online @ www.nejm.org.//
9. Levy, D., Anderson, S.B., Christiansen, J.C., el al. Determinants of sensitivity and specificity of electrocardiographic criteria for left ventricular hypertrophy.  Amer. H. Assoc. Scientific Division,   Circulation.  (1990); 81:  815-820. www.circulation.org.// http://intl.ahajournals.org
10. Fuster, V., Alexander, W.R., O’Rourke, R.A., et al.  Hurst’s The Heart (11th ed.) vol. 1, part 2 Chapter 13, pp.310-325. New York:  McGraw-Hill Co. Inc. Medical Textbook Division.
11. Casale,P.N., Devereux, R.B., Kligfield, P.,  et al.  Electrocardiographic detection of left ventricular hypertrophy:  Development and prospective validation of improved criteria. J. Amer. Coll. Cardio.  (1995); 6: 572-578. Cited in http://www.jmcc.org//
12. Levy, D., Labib, S.B., Anderson, K.M., Christiansen, J.C., et al. Amer. H. Assoc. Scientific Division,  Circulation.  (1990) 81:  815-820.
13. Levine H.D., Wanzer, S.H., Merrill, J.P. Dialyzable currents of injury in potassium intoxication resembling acute myocardial infarction or pericarditis. Cited in the Amer. H. Assoc. Scientific Journal, Circulation.  (1995)13: 29-36.
14. Fisch, C. Electrocrocardiography and vectorcardiography.  In:  Braunwald E., ed. Heart Disease, 4th ed. Medical Textbook Philadelphia:  Saunders; 1992:  116-120.
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16. Mc Lenachan, J.M., Henderson, E., Morris, K.I., Dargie, H.J. Ventricular arrhythmias in patients with hypertensive left ventricular hypertrophy.   N. Engl. J. Med. (1987); 317: 787-792. Reprint in:  N. Engl. J. Med. (2005) back issue online @ www.nejm.org.// The New England Journal of Medicine is owned, published, and copyrighted © 2009 Massachusetts Medical Society
17. Bonow, R.O., Bohannon, N, Hazzard, W. Risk stratification in coronary artery disease and special populations [published erratum appears in:  Amer. J. Med. (1997); 102: 322].  Cited in http://www.amjmed.com.// (suppl. 4A): 17S-24S.
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20. Chen, JTT. Cardiac fluoroscopy:  In: Kelley MJ ed. Symposium on chest radiography for the cardiologist.  Cardiol. Clin. (1983); 1: 565-573.
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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 the Blackwell Publishing Co. (Medical Division), and Journal of American College of Cardiology, plus 15 published abstracts within 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.


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 professional consultation, please use e-mail address: [email protected]

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