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Basic Cardiac Assessments:  Physical

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-
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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. 3’4 

     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
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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. 
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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
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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
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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
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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.

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  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.