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10: CARDIOVASCULAR GUIDELINES
g. Antidepressants (tricyclic antidepressants) and
selective serotonin reuptake inhibitors: major adverse
cardiovascular events, including HF, MI, stroke, and
cardiovascular death.
h. Phosphodiesterase inhibitors (PDE-3, PDE-4, and
PDE-5): increased mortality.
i. Antiarrhythmic: Negative inotropic activity and fur-
ther reduction in LV function can impair the elimination and result in toxicity of the antiarrhythmic agent.
j. Chemotherapy: Many are cardiotoxic.
k. Androgen–testosterone patch: Edema may increase
the rate of HF.
l. Theophylline-serum levels may increase and cause
toxicity due to acute decompensation of HF.
m. Sodium bicarbonate and Fleet Phospho-Soda con-
tain signicant quantities of sodium.
n. Herbal/supplements may also affect HF.
4. Pneumonia vaccination and annual inuenza immuni-
zation should be encouraged.
FOLLOW-UP
A. HF clients should be comanaged with a cardiologist.
B. Close follow-up is essential if the client is to be maintained
as an outpatient.
C. Appointments every 1 to 2 weeks may be necessary, with
additional appointments depending on the client’s symptoms, such as increasing SOB, inability to lie at to sleep, nocturnal moist cough, and increase in daily weight.
D. Laboratory monitoring is required for electrolytes, blood
urea nitrogen, creatinine, proteinuria, and digoxin level.
CONSULTATION/REFERRAL
A. Consult a physician when the client requires the next level
up in pharmacologic management.
B. Consult a cardiologist for staging and hospital
management.
INDIVIDUAL CONSIDERATIONS
A. Pregnancy:
1. HF is uncommon in healthy females without coexist-
ing heart disease.
2. Pregnancy in a client with heart disease is considered
high risk.
3. Refer to a high-risk obstetrician/perinatologist for care
during pregnancy.
B. Pediatrics:
1. HF is usually associated with congenital heart defects.
C. Adults:
1. The 5-year survival rate is 25% for males and 38% for
females.
2. Predictors of poor outcome include an EF less than
25%, ischemic etiology, ventricular arrhythmias, serum
sodium less than 130 mEq/L, poor functional class, low
cardiac index, and high lling pressures.
D. Geriatrics:
1. In very frail elderly clients or those in long-term care
settings, the only sign may be increased agitation or acute
change in level of consciousness.
BIBLIOGRAPHY
American Heart Association. (2017). Top ten things to know: 2017 ACC/AHA/
HFSA focused update of the 2013 ACCF/AHA guideline for the management of heart failure. https://www.heart.org/-/media/data-import/
downloadables/hfsa-focused-update-for-the-management-of-heartfailure-ucm_493382.pdf
Colucci, W., & Borlaug, B. (2021). Heart Failure: Clinical manifesta-
tions and diagnosis in adults. Up To Date. https://www.uptodate.
com/contents/heart-failure-clinical-manifestations-and-diagnosisin-adults?search=heart%20failure%20&source=search_result&
selectedTitle=18~150&usage_type=default&display_rank=18#H22
Murphy, N., Shanks, M., & Alderman, P. (2019, January). Management of
heart failure with outpatient technology. Journal for Nurse Practitioners,
15(1), 12–18. https://doi.org/10.1016/j.nurpra.2018.07.004
HYPERTENSION
DEFINITION
A. Discord exists between the American College of Cardiology/
American Heart Association (ACC/AHA) (2017) and the Joint
National Committee (JNC) 8 guideline (2014) as to the denition and stages of hypertension (HTN). The JNC 8 guideline
provided more permissive (higher) blood pressure (BP) goals,
especially for those 60 and older. The newer AHA/ACC guideline denes HTN as an systolic blood pressure (SBP) of 130
mmHg or more, a diastolic blood pressure (DBP) of 80 mmHg or
more, or describes a condition in which a person is taking antihypertensive medications (Table 10.6; for more information go
to www.ahajournals.org/doi/10.1161/HYP.0000000000000065).
B. Resistant HTN is dened as:
1. BP that is not at target despite a three-drug regimen,
with one of the agents being a diuretic appropriate for the
client’s glomerular ltration rate (GFR).
2. BP that is controlled while taking four or more medica-
tions is also considered resistant HTN.
C. Standing and supine BPs should be measured before
the initiation of combination antihypertensive therapy.
Orthostatic (postural) hypotension is diagnosed when, within
2 to 5 minutes of quiet standing, one or more of the following
is present:
1. At least a 20 mmHg fall in systolic pressure.
2. At least a 10 mmHg fall in diastolic pressure.
3. Symptoms of cerebral hypoperfusion, such as
dizziness.
D. The average nocturnal BP is approximately 15% lower
than daytime values. Failure of the BP to fall by at least 10%
during sleep is called “nondipping” and is a stronger predictor of adverse cardiovascular outcomes than daytime BP.
E. Isolated systolic HTN (ISH) is when the SBP is greater than
or equal to 130 mmHg, with DBP normal or below normal
(<80 mmHg). ISH usually affects the elderly, increasing their
risk of stroke or myocardial infarction (MI).
F. Isolated diastolic HTN (IDH) is dened as a diastolic pres-
sure greater than or equal to 80 mmHg, with a systolic pressure less than 130 mmHg. IDH is more common in younger
males who are overweight/obese and in individuals younger
than 40 years.
G. Malignant HTN is marked HTN with retinal hemorrhages,
exudates, or papilledema. It is usually associated with pressures above 180/120 mmHg, with evidence of end-organ
damage.
INCIDENCE
A. Worldwide, HTN affects about 975 million people.
B. Approximately 75 million people, equivalent to one in
three adults, in the United States have HTN.
C. The incidence of resistant HTN is being studied more
closely; the current rate is about 12% of all clients with HTN.
D. High BP was a primary or contributing cause of death for
more than 410,000 Americans in 2014—that is more than 1,100
deaths each day.
TABLE 10.6 WHELTON 2017 HIGH BP CLINICAL PRACTICE GUIDELINE
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HYPERTENSION
299
Ethnicity/Population
General population ≥60
Clients with chronic kidney
disease
Clients with chronic kidney
disease (regardless of race or
diabetes status)
Clients with diabetes ≥18
Age
(Years)
<60
≥18
≥18
Begin Initiation of
Pharmacologic Treatment to
Lower BP
Initiate therapy for SBP ≥130
mmHg or DBP ≥80 mmHg.
Initiate therapy to lower BP at SBP
≥130 mmHg.
Initiate therapy to lower BP at DBP
≥80 mmHg.
Initiate therapy to lower BP at
SBP ≥130 mmHg or DBP ≥80
mmHg.
Initiate therapy to lower BP at
SBP ≥130 mmHg or DBP ≥80
mmHg.
BP Goals for
Treatment
Treat to goal of SBP
<130 mmHg and
DBP <80 mmHg.
Treat to goal of SBP
<130 mmHg.
Treat to goal of DBP
<80 mmHg.
Treat to goal of SBP
<130 mmHg and
DBP <80 mmHg.
Treat to goal of SBP
<130 mmHg and
DBP <80 mmHg.
Other Comments
If pharmacologic treatment
results in a lower achieved
SBP and treatment is
well-tolerated, treatment does
not need to be adjusted.
Initial or add-on antihypertensive
therapy should include an
ACEI or ARB to improve
kidney outcomes.
The American Diabetes
Association criteria differ
from all others in that these
guidelines advocate treating
toward an SBP goal of <140
mmHg and to a DBP of <80
mmHg.
General non-Black population,
including those with diabetes
General Black population,
including those with diabetes
ACEI, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; BP, blood pressure; CCB, calcium channel blocker; DBP, diastolic blood pressure; SBP,
systolic blood pressure.
Source: Data from Whelton, P. K., Carey, R. M., Aronow, W. S., Casey Jr, D. E., Collins, K. J., Himmelfarb, C. D., DePalma, S. M., Gidding, S., Jamerson, K. A., Jones, D.
W., MacLaughlin, E. J., Muntner, P., Ovbiagele, B., Smith Jr, S. C., Spencer, C. C., Stafford, R. S., Taler, S. J., Thomas, R. J., Williams Sr, K. A., . . . Wright Jr, J. T. (2017).
ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/MNA/PCN guideline for the prevention, detection, evaluation, and management of high blood pressure in adults.
Hypertension. https://doi.org/HYP.0000000000000065.
PATHOGENESIS
A. More than 90% of cases have no identiable cause, thus
constituting the category of primary or essential HTN. The
remaining 10% of cases have the following secondary causes:
1. Renal causes:
a. Glomerulonephritis.
b. Pyelonephritis.
c. Polycystic kidney disease.
2. Endocrine causes:
a. Primary hyperaldosteronism.
b. Pheochromocytoma.
f. Corticosteroids.
g. Lithium.
h. Ergotamine alkaloids.
i. Cyclosporine.
j. Monoamine oxidase inhibitors (MAOIs), in combi-
nation with certain drugs or foods.
k. Appetite suppressants, in combination with certain
drugs or foods.
l. Cocaine.
m. Amphetamines.
5. OSA.
Initial antihypertensive therapy
should include a thiazide-type
diuretic, CCB, ACEI, or ARB.
Initial antihypertensive therapy
should include a thiazide-type
diuretic and CCB.
c. Hyperthyroidism.
d. Cushing syndrome.
3. Vascular causes:
a. Coarctation of aorta.
b. Renal artery stenosis.
4. Chemical/medication-induced:
a. Oral contraceptives.
b. Nonsteroidal anti-inammatory drugs (NSAIDs).
c. Decongestants.
d. Antidepressants.
e. Sympathomimetics.
PREDISPOSING FACTORS
A. When making a diagnosis, consider not only the absolute
BP reading, but also the presence or absence of other cardiovascular risk factors (Table 10.7). Factors include the following:
1. Family history of HTN.
2. Obesity.
3. Alcohol consumption.
4. Stress.
5. Sedentary lifestyle.
6. African American ancestry.
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10: CARDIOVASCULAR GUIDELINES
TABLE 10.7 MODIFIABLE AND NONMODIFIABLE
RISK FOR CONTROL OF HYPERTENSION
Modifiable Nonmodifiable
Sedentary lifestyle Age
Smoking Sex
Diet Ethnicity
Lipid control Diabetes
Sodium intake Postmenopausal
Alcohol intake Family history
Obesity
7. Male.
8. Age greater than 30 years.
9. Excessive salt intake.
10. Medications.
11. Drug use.
COMMON COMPLAINT
A. HTN is asymptomatic in the majority of clients.
OTHER SIGNS AND SYMPTOMS
A. Headaches.
B. Advanced disease: organ-specic complaints with
end-organ damage.
C. Retinopathy.
POTENTIAL COMPLICATIONS
A. Cerebral vascular accident (CVA).
B. MI.
C. Renal failure.
D. Heart failure (HF).
E. Peripheral arterial disease (PAD).
SUBJECTIVE DATA
A. Ask the client about any family history of HTN or cardiac
or renal disease.
B. Ask if the client has ever been diagnosed with HTN or car-
diac or renal disease.
C. Ask if the client ever had any high BP readings.
D. Ask if the client has ever been treated for any of the afore-
mentioned problems.
E. Ask the client about other risk factors such as smoking,
drinking, high-fat intake, obesity, and/or diabetes.
F. Inquire about the client’s lifestyle, exercise regimen, work
environment, and stress level.
G. Ask the client about symptoms that suggest secondary
etiology:
1. Palpitations, headache, diaphoresis (pheochromo cytoma).
2. Anxiety, weight gain or loss (thyroid abnormality).
3. Muscle weakness, polyuria (primary
hyperaldosteronism).
H. Find out if the client is taking drugs that elevate BP (noted
under the “Pathogenesis” section).
I. Ask whether the client feels nervous when having their BP
taken in the ofce (“white coat HTN”).
J. Review current medications, including prescription,
over-the-counter (OTC), and herbal products.
K. Review current recreational/illicit drug use.
PHYSICAL EXAMINATION
A. Check pulse, BP, height, weight, waist circumference, and
distribution of body fat. Calculate the body mass index.
1. The diagnosis of HTN is made after averaging two or
more properly measured readings at each of two or more
visits after an initial screen. Compare both upper extremes
during the rst visit; if they are unequal, use the higher
value.
2. When the client’s SBP and DBP fall into two different
categories, use the higher category to classify their BP.
3. For accurate measurement, use the correct size cuff for
the client (adult, large adult, or thigh cuff). Compare the
home cuff’s reading with the ofce cuff’s reading to verify
the accuracy of the home cuff’s measurements.
4. Perform manual vital signs with irregular rhythms.
5. If there are still problems diagnosing true HTN, con-
sider a 24-hour ambulatory BP monitor.
B. Inspect:
1. Observe overall appearance.
2. Conduct funduscopic examination; look for papill-
edema, exudates, arteriovenous nicking, anterior nicking.
3. Inspect the neck for jugular vein distention.
4. Observe for lower extremity edema.
C. Auscultate:
1. Heart: Note the point of maximal impulse.
2. Lungs: Check for bronchospasm and rales.
3. Neck: Assess carotid arteries for bruits.
D. Palpate:
1. Palpate the neck; check thyroid for enlargement.
2. Palpate the abdomen for masses or organomegaly.
3. Palpate the extremities; assess peripheral pulses and
note edema.
4. Assess deep tendon reexes (DTRs).
DIAGNOSTIC TESTS
A. Hematocrit.
B. Liver function tests, lactate dehydrogenase (LDH) test,
and uric acid test.
C. Chemistry prole.
D. Lipid prole (total and high-density lipoprotein choles-
terol and triglycerides).
E. Urinalysis for proteinuria.
F. Estimated GFR.
G. EKG.
H. If history, physical examination, or laboratory tests indi-
cate the need, obtain the following:
1. Intravenous pyelography (IVP).
2. Renal arteriogram.
3. Plasma renin.
4. Catecholamines.
5. Chest radiography.
6. Aortogram.
7. Ultrasonography.
8. Sleep study.
I. Monitor potassium levels if client is on an
angiotensin-converting enzyme inhibitor/angiotensin receptor blocker (ACEI/ARB) or spironolactone.
DIFFERENTIAL DIAGNOSES
A. Primary HTN.
B. Secondary HTN.
C. Drug-induced HTN.
D. White coat syndrome.
HYPERTENSION
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301
PLAN
A. General interventions (Table 10.7):
1. Advise overweight clients to lose weight. Loss of as lit-
tle as 10 lbs reduces BP in many clients.
2. Advise the client to limit or discontinue alcohol intake.
3. Encourage the client to stop smoking.
4. Encourage increased physical activity. The 2017 ACC/
AHA guidelines on lifestyle management outline the optimal physical activity recommendation, which advises
adults to engage in 40 minutes of aerobic physical activity
three to four times a week (Table 10.7). The aerobic exercise
should involve moderate to vigorous intensity.
5. Encourage some form of relaxation technique.
B. Client teaching:
1. Stress the asymptomatic nature of the disease.
2. Stress the importance of ongoing monitoring and treat-
ment under the direction of a healthcare provider.
3. Review risk factors for cardiac, renal, and cerebrovas-
cular disease and possible preventive measures.
4. The ACC maintains the CardioSmart Patient
Education Portal as an online BP management tool
to educate and motivate clients. ACC’s CardioSmart
is a free resource found at www.cardiosmart.org.
CardioSmartTXT PREVENT is a 6-month program of
health tips and reminders sent via two text messages a
week. CardioSmartTXT QUIT is a 2-month program to
assist clients in smoking cessation. Four text messages are
sent a day with information and assistance with smoking
cessation. Clients can sign up at author.cardiosmart.org/
Tools/CardioSmartTXT-Prevent.
C. Dietary management:
1. Review specic dietary measures. Give dietary rec-
ommendation sheets. See Appendix B for low-fat/
low-cholesterol and dietary approaches to stop HTN.
2. Diet alone will make only the lowest incremental
change in BP; therefore, it should be combined with lifestyle modication. Lower sodium intake, smoking cessation, weight loss, and exercise are all essential.
3. It is essential for the client/family to read labels for
sodium, fat content, and serving sizes.
4. Other dietary changes include low-fat/low-cholesterol
diets and limiting fat consumption.
a. Use monounsaturated fats to reduce cholesterol:
i. Canola oil.
ii. Olive oil.
b. Use polyunsaturated fats in limited quantities:
Polyunsaturated fats reduce cholesterol, but not as
well as monounsaturated fats:
i. Vegetable and sh oils.
ii. Corn, safower, peanut, and soybean oils.
c. Limit saturated fats:
i. Animal fats and some plant fats.
ii. Butter and lard.
iii. Coconut oil and palm oil.
D. Pharmaceutical therapy:
1. If lifestyle changes alone are not adequate to control
HTN, consider drug therapy. Medication doses are dependent on age, ethnicity, and comorbid conditions. Most clients will require two or more medications to control their
BP. Consider starting antihypertensives and/or diuretics
(see Table 10.5 for drugs and classications) as outlined by
the current guidelines. An extensive guideline is available
at www.thecardiologyadvisor.com/home/clinical-charts/
hypertension-treatment-algorithm.
2. The 2017 Science Advisory recommendations from
the AHA, ACC, and the Centers for Disease Control and
Prevention provide medication classications for treatment
of HTN in the presence of medical conditions (Table 10.8).
3. ACEIs, ARBs, calcium channel blockers (CCBs), and
thiazide diuretics should be used as rst-line options,
either as single agents or in combination.
4. Antihypertensives/diuretics should be started at low
doses and then the doses increased if there is inadequate
response to initial therapy and nonadherence is ruled out.
Consider the following:
a. Increasing drug dose.
b. Substituting another drug.
c. Adding a second drug from another class; a diuretic
is recommended if one is not already being used.
d. Beta-blockers are no longer rst-line antihyperten-
sive agents. A beta-blocker can be used in clients who
have any of the following: coronary artery disease,
post-MI, dysrhythmia, and HF. Those older than 60
years, however, should not use a beta-blocker as the
initial agent. Atenolol should not be used for HTN
treatment as it has been shown to be less effective in the
prevention of events compared with all other agents.
e. ACEIs and ARBs are critical medications to prescribe
and titrate to maximum dose as a rst-line medication
in people with renal disease, diabetes, and proteinuria.
5. If response is still inadequate, add a second or third
drug or a diuretic if one has not already been tried.
6. Evaluate the client for secondary causes if severe HTN
is resistant to therapy.
7. Resistant HTN: Rule out all inadequate responses to
the three-drug therapy (ACEI or ARB or CCB + diuretic):
a. “White coat HTN”: Have the client begin to take
and record their BP at home and report the values.
b. Use size-appropriate BP cuffs on obese clients.
c. Nonadherence to therapy, including side effects, med-
ication regimen too complex, and/or cost/affordability.
d. Volume overload due to excessive salt intake, pro-
gressive renal damage, uid retention from BP reduction, and inadequate diuretic therapy.
e. Drug problems: dose too low, wrong type of diuretic,
inappropriate combinations, rapid inactivation, drug
actions, and interactions.
f. Associated conditions: smoking, obesity, sleep
apnea, insulin resistance, ethanol intake more than
30mL (1 oz) per day, panic attacks, chronic pain, and
organic brain syndrome.
g. Adding spironolactones can decrease SBP by 25
mmHg on average and DBP by 12 mmHg on average
in clients with resistant HTN.
8. Treat with decongestants very cautiously.
Pseudoephedrine HCl (Sudafed) has the least cardiovascular effect.
9. Diuretics may worsen gout and diabetes.
10. Beta-blockers are contraindicated in clients with
asthma, HF, and heart block.
11. Use diltiazem HCl (Cardizem) and verapamil HCl
(Calan) cautiously in clients with HF or block
12. ACEIs may cause coughing.
13. Abrupt cessation of therapy with a short-acting
beta-blocker, such as propranolol, or the short-acting alpha-2
agonist clonidine can lead to a potentially fatal withdrawal
syndrome. Gradual discontinuation of these agents over a
period of weeks should prevent this syndrome.
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TABLE 10.8 AHA, ACC, AND CDC 2013 SUGGESTED HYPERTENSIVE MEDICATIONS BY MEDICAL
CONDITION
Medical Condition BB ACEI or ARB Aldo Antag Thiazide CCB
Coronary artery disease/post-MI X X
Systolic heart failure X X X X
Diastolic heart failure X X X
Diabetes X X X X
Kidney disease X
Stroke or TIA ACEI X
ACC, American College of Cardiology; ACEI, angiotensin-converting-enzyme inhibitor; AHA, American Heart Association; Aldo Antag, aldosterone antagonist; ARB, angiotensin
II blocker; BB, beta-blocker; CCB, calcium channel blocker; CDC, Centers for Disease Control and Prevention; MI, myocardial infarction; TIA, transient ischemic attack.
14. A suggested treatment protocol for moderate HTN of
>20mmHg above goal is:
15. If HTN is not controlled, the following may be added
in stepwise order:
16. Differences in ARBs and diuretics:
10: CARDIOVASCULAR GUIDELINES
a. An ACE inhibitor or an ARB with a diuretic or a
dihydropyridine (DHP) CCB (e.g., amlodipine, felodipine, or nifedipine) combination.
b. Start with a low dose and titrate upward.
a. A DHP CCB or a thiazide diuretic (chlorthalidone
is more potent than hydrochlorothiazide [HCTZ]; add
whichever has not yet been used); can use combination
low-dose amiloride/HCTZ in appropriate clients.
b. A vasodilating beta-blocker (e.g., carvedilol or
nebivolol) and/or an aldosterone blocker.
c. Alpha-blockers and direct vasodilators.
d. Consider referral to HTN specialist.
a. Losartan (Cozaar) is weakest ARB; may require
E. Home and ambulatory blood pressure monitoring (ABPM)
is an adjunctive tool for the management of HTN.
1. BP tracking apps are available at online app stores for
smartphones, MP3 players, and tablets.
2. The AHA/American Stroke Association has BP tracker
instructions found at www.heart.org/idc/groups/
heart-public/@wcm/@hcm/documents/downloadable/
ucm_305157.pdf.
3. A printable BP tracker log is found at www.organized
home.com/sites/default/les/image/pdf/health_blood
_pressure_tracker.pdf.
F. Consider a sleep study for the diagnosis of OSA (see
“Obstructive Sleep Apnea” section in Chapter 9).
G. Clients with pre-HTN without diabetes, chronic kidney
disease (CKD), or cardiovascular disease should be treated
with nonpharmacologic therapy (e.g., diet, sodium reduction,
weight loss, exercise, smoking cessation) and should be evaluated annually.
twice a day dosing.
b. More potent ARBs include olmesartan and azilsar-
tan (most potent).
c. Chlorthalidone is more potent than HCTZ.
17. For HTN that is difcult to treat:
a. Make sure client is on a sodium-restricted diet of
1,500mg to 2,000 mg of sodium per day and not taking
OTC NSAIDs or drinking excessively.
b. If a client is already on an ACEI or ARB with a thia-
CONSULTATION/REFERRAL
A. If the client is pregnant, consult a physician before pre-
scribing medications. Many antihypertensive drugs are harmful to the fetus.
B. Consult a physician if the client is having an acute hyper-
tensive emergency: DBP greater than 130 mmHg.
C. Consult/comanage with a physician if the client needs
more than three drugs for therapy.
zide diuretic and SBP remains elevated, rst try changing ACEI to ARB; if on losartan, try changing to a more
potent once-daily ARB.
c. If the client is already on a beta-blocker for another
reason, may change to a vasodilating beta-blocker.
d. If the client is on HCTZ, change to chlorthalidone,
which is a more potent diuretic.
e. May add an aldosterone blocker if BP remains
uncontrolled.
f. May add a DHP CCB.
INDIVIDUAL CONSIDERATIONS
A. Pregnancy: Refer to Chapter 13, “Obstetrics Guidelines.”
1. HTN may be either chronic or pregnancy-induced.
2. HTN is considered chronic if it is present before preg-
nancy or diagnosed before the 20th week of gestation.
3. Pregnancy-induced hypertension is diagnosed if SBP
increases 30 mmHg or more or if DBP increases 15 mmHg
or more over baseline when compared with BP readings
before the 20th week of gestation. When BP readings are
not known, a reading of 140/90 mmHg or higher is con-
FOLLOW-UP
A. If drug therapy is initiated, see the client again in 2 to 4
weeks for follow-up.
B. Once the client is stable, see them every 3 to 6 months.
C. Evaluate the client yearly, including uric acid, creatinine,
and potassium.
D. Review and discuss drug therapy compliance, effective-
ness, and adverse reactions (including effect on sexual activity) at each visit.
sidered abnormal.
4. Maternal as well as fetal mortality and morbidity
improve with treatment.
B. Pediatrics:
1. Evaluate BP at every visit starting at the age of 3 years.
2. HTN can occur in many acute illnesses, or it may be a
chronic problem.
3. Determine high BP by correlating height indexes with
BP readings.
LYMPHEDEMA
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C. Geriatrics:
1. The optimal BP treatment goal in the elderly has not
been determined, as there is no consensus among various national and international organizations. In the most
recent JNC 8 guideline, treatment goals for individuals
older than 60 years were changed to a goal of less than
150/90 mmHg. HTN in the elderly places the client at risk
of coronary events, stroke, HF, and PAD.
2. Elderly persons with HTN are more likely to develop
orthostatic and postprandial hypotension, which may
result in falls or syncope.
a. Evaluate side effects, including dizziness and
sedation.
b. Beta-blockers may cause depression or confusion in
the elderly.
3. The general approach to drug therapy in the geriatric
population is to start low and go slow.
4. Check the Beers list for harmful drugs in the geriatric
population. The 2019 American Geriatrics Society’s Updated
Beers Criteria for Potentially Inappropriate Medication Use
in Older Adults is available at geriatricscareonline.org/
ProductAbstract/american-geriatrics-society-updatedbeers-criteria-for-potentially-inappropriate-medicationuse-in-older-adults/CL001. A printable pocket card is
available for download at www.americangeriatrics.org/
publications-tools.
5. To avoid hyperkalemia in the elderly, potassium-sparing
diuretics should not be given with ACEI or ARBs.
RESOURCE
The National Kidney Foundation provides online calculators: www.kid-
ney.org/professionals/KDOQI/gfr_calculator
BIBLIOGRAPHY
Davis, L. L. (2019, January). Hypertension: How low to go when treating
older adults. Journal for Nurse Practitioners, 15(1), 1–6. https://doi.org
/10.1016/j.nurpra.2018.10.010
James, P. A., Oparil, S., Carter, B. L., Cushman, W. C., Dennison-Himmelfarb,
C., Handler, J., & Ortiz, E. (2014). 2014 evidence-based guideline for
the management of high blood pressure in adults: Report from the
panel members appointed to the Eighth Joint National Committee
(JNC 8). Journal of the American Medical Association, 311(5), 507–520. htt
ps://doi.org/10.1001/jama.2013.284427
Whelton, P., & Carey, R. (2018). ACC/AHA/AAPA/ABC/ACPM/ AGS/
APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention,
Detection, Evaluation, and Management of High Blood Pressure in
Adults A Report of the American College of Cardiology/American
Heart Association Task Force on Clinical Practice Guideline. Journal of
the American College of Cardiology, 71, e127–248.
LYMPHEDEMA
DEFINITION
A. Peripheral vascular disease (PVD) is a general term that
encompasses all occlusive or inammatory diseases that
occur within the peripheral arteries, veins, and lymphatic system. Lymphedema is a chronic condition caused by the accumulation of lymphatic uid in the interstitial tissue.
INCIDENCE
A. The Vascular Disease Foundation reports that almost one
million Americans have lymphedema. The incidence worldwide is projected to approach 100 million.
PATHOGENESIS
A. Lymphedema occurs when lymph uid is unable to ow
in a normal manner and accumulates in an extremity. The
propensity for lymphedema can be inherited or caused by
another condition, such as lymphangitis, malignancy, lariasis, removal of lymph nodes, and major trauma or burns.
PREDISPOSING FACTORS
A. Cancer.
B. Radiation therapy.
C. Surgical removal of lymph nodes.
D. Parasitic infection (lariasis).
E. Congenital disorders involving the structure of the lymph
system:
1. Milroy disease.
2. Meige disease.
F. Obesity.
G. Surgical implantation of pacemaker or arteriovenous
shunt.
H. Systemic diseases (hyperthyroidism, hypertension, renal
or cardiac disease).
I. Vascular disease (chronic venous insufciency [CVI] or
postthrombotic syndrome).
J. Sedentary lifestyle.
COMMON COMPLAINTS
A. Severe edema that is consistent to the distal aspect of the
extremity.
B. Hard skin over edematous area.
C. Loss of range of motion.
POTENTIAL COMPLICATIONS
A. Infection, including lymphangitis and cellulitis.
B. Lymphangiosarcoma.
SUBJECTIVE DATA
A. Ask the client when the symptom were rst noticed.
B. Have the client describe the duration of symptoms.
C. Review any history of cancer, radiation, and chemotherapy.
D. Review recent history of invasive procedures or surgery.
E. Ask the client to list all medications currently being taken,
particularly substances not prescribed and illicit drugs.
F. Ask the client to describe any pain.
G. Ask the client what makes the symptoms better and what
makes them worse.
H. Have the client rate discomfort on a scale of 1 to 10, with 1
being the least uncomfortable.
PHYSICAL EXAMINATION
A. Check vital signs: blood pressure, resting heart rate, respi-
rations, temperature, height, weight, and body mass index.
B. Inspect:
1. Assess for signs of erythema, increased temperature,
and edema.
C. Auscultate:
1. Heart: rate, rhythm, heart sounds, murmur, rub, and
gallops.
2. Lungs: lung sounds in all elds.
D. Palpate:
1. Lymph nodes distal and proximal to the site.
2. Pulses distal and proximal in all extremities.
3. Extremity for tenderness.
DIAGNOSTIC TESTS
A. Serum laboratory tests: complete blood count (CBC) with
differential and brain natriuretic peptide (BNP).
B. CT scan of the affected extremity.
C. Doppler ultrasound of the affected extremity.
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D. MRI.
E. Lymphoscintigraphy.
F. Additional tests to monitor coexisting systemic and/or
vascular disease.
DIFFERENTIAL DIAGNOSES
A. Unilateral limb edema:
1. Lymphedema.
2. Venous insufciency.
3. Deep vein thrombosis or postthrombotic syndrome.
4. Arthritis.
5. Baker cyst.
6. Presence or reoccurrence of cancer.
B. Symmetrical limb edema:
1. Congestive heart failure (CHF).
2. CVI.
3. Renal dysfunction.
4. Hepatic dysfunction.
5. Hypothyroidism (myxedema).
6. Medication-induced edema.
7. Lipedema.
PLAN
A. General interventions:
1. Protect the arm or leg while recovering from cancer
treatment.
2. Suggest strategies to protect the extremity from devel-
oping a blood clot.
B. Client teaching: See Client Teaching Guide for this chapter,
“Lymphedema.”
1. Avoid heavy lifting, if an arm is affected.
2. Avoid strenuous exercise.
3. Avoid heat on the arm or leg.
4. Avoid tight clothing.
5. Inspect the affected limb daily. Note any cracks or cuts
that increase the risk of infection and treat as directed.
6. Apply lotion daily to protect and prevent dry skin.
7. Avoid burns to the skin.
8. Take extra care when shaving and use a clean razor on
clean skin.
9. Use insect repellent to prevent insect bites, which could
become infected.
10. Wash skin daily with a mild soap and dry skin care-
fully paying special attention to any skin folds.
11. Prevent excessive sun exposure by applying sunscreen
or wear appropriate clothing to cover skin.
C. Nonpharmaceutical therapy: consists of two phases of
complex decongestive therapy (CDT).
1. Intensive reduction phase:
a. Duration: usually lasts 2 to 4 weeks for severe
lymphedema. If lymphedema is mild to moderate, it is
possible to skip to the maintenance phase of theCDT.
b. Steps of CDT in the intensive reduction phase:
i. Low-stretch bandages (an adjustable compres-
sion garments).
ii. Manual lymphatic drainage (MLD) —MLD
consists of gentle, skin-stretching movements performed by a certied therapist.
iii. Sequential gradient pump—Durable medical
equipment that provides gentle massage that mimics MLD.
iv. Exercises—A physical therapy referral for a
home exercise plan would be appropriate. A home
exercise plan would likely include resistance bands
or light weights and walking.
v. Skincare and risk precautions:See the “Client
Teaching” section.
2. Maintenance phase:
a. Duration: lifelong, although the frequency of treat-
ments can be tailored to the symptoms.
b. Steps of CDT in the maintenance phase:
i. Compression garments.
ii. Exercises in the form of a home exercise plan.
iii. Skincare and risk precautions: See the “Client
Teaching” section.
iv. Manual lymphatic drainage, if required.
v. Sequential gradient pump, if required.
D. Surgery:
1. Lymphaticovenous anastomosis (LVA): the surgical
attachment of nonfunctional lymph nodes to the venous
system thereby allowing for drainage of access uid.
2. Vascularized lymph node transfer (VLNT): the trans-
plantation of functional lymph nodes into an extremity to
restore lymphatic function.
3. Suction assisted protein lipectomy (SAPL): a treatment
in which suction is used to remove lymphatic solids and
fatty deposits. This surgery is most commonly used to treat
those who are poor candidates for LVA and/or VLNT.
FOLLOW-UP
A. Follow-up is determined by the client’s needs, frequency
and intensity of symptoms, and presence of other medical
conditions.
B. When PVD manifests with persistent symptoms, it must
be followed by a cardiologist.
CONSULTATION/REFERRAL
A. When acute limb ischemia (ALI) is suspected, refer the cli-
ent for immediate hospitalization to obtain diagnostic testing
to determine the presence of a thrombus and restore circulation to the affected extremity.
B. If chronic limb ischemia (CLI) has led to ulceration and/
or superimposed infection, then hospitalization is indicated to
initiate a wound care consultation, along with diagnostic testing to determine the degree of arterial occlusion.
C. Referral to a cardiologist is indicated in the presence of
persistent PVD.
D. Referral to a certied lymphedema therapist to manage
chronic lymphedema.
E. Referral to physical therapy is indicated to teach a home
exercise program.
BIBLIOGRAPHY
Executive Committee of the International Society of Lymphology.
(2020). The diagnosis and treatment of peripheral lymphedema: 2020
Consensus Document of the International Society of Lymphology.
Lymphology, 51(1), 3–19. https://pubmed.ncbi.nlm.nih.gov/32521126/
Schaverien, M. V., Moeller, J. A., & Cleveland, S.D. (2018, February).
Nonoperative treatment of lymphedema. Seminars in Plastic Surgery,
32(1), 17–21. https://doi.org/ 10.1055/s-0038-1635119
Vascular Cures. (2017). What is Lymphedema? https://vascularcures.org/
lymphedema/
MURMURS
DEFINITION
A. A murmur is turbulent blood ow through the heart as a
result of one or more of the following etiologies:
1. Narrow valve opening, stenosis.
2. Incomplete valve closure, regurgitant, or insufcient
blood ow.
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3. Abnormal opening through chambers, atrial or ven-
tricular septal defect (VSD).
4. Rapid blood ow through normal valve structures;
occurs during pregnancy, with increased physiologic
demand states, and in children.
5. No abnormality; occurs in clients with thin chest walls
and in children.
INCIDENCE
A. Approximately 80% of children have a physiologic mur-
mur at one time or another. Of the females studied in the
Framingham Heart Study, 4% had a murmur related to mitral
valve prolapse (MVP).
PATHOGENESIS
A. Pathogenesis depends on specic etiology, but rheumatic
disease, calcic changes, ischemic insults, congenital abnormalities, and degenerative diseases all contribute to the development of a murmur.
COMMON COMPLAINTS
A. Often no symptoms are present, and murmur is found on
routine examination.
B. Complaints with advanced valvular disease:
1. Chest pain.
2. Dyspnea.
3. Palpitations.
4. Shortness of breath (SOB).
5. Exercise intolerance.
6. Postural light-headedness.
SUBJECTIVE DATA
A. Has the client ever been diagnosed with a murmur?
B. Did the client have frequent strep infections as a child?
C. Ask the client about any recent viral infections.
D. Question the client about chest pain, SOB, palpitations,
diaphoresis, light-headedness, or syncope, especially with
exertion.
E. Ask the client whether any family members had sudden
cardiac death before the age of 55 years.
PHYSICAL EXAMINATION
A. Check temperature, if indicated, pulse, respirations, and
blood pressure.
B. Inspect:
1. Chest for lifts and heaves.
C. Palpate:
1. Chest for lifts, heaves, and thrills.
D. Auscultate:
1. Heart for splitting of heart sounds, clicks, rubs, and mur-
murs; use the bell and diaphragm of the stethoscope to auscultate the client in the left lateral, supine, standing, sitting
(and leaning forward), and squatting positions and after having them run in place or do jumping jacks for 2 to 3 minutes.
a. A new, systolic, regurgitant murmur in the setting of
an acute myocardial infarction (MI) may indicate a ruptured papillary muscle and possible cardiogenic shock.
b. When a new murmur is audible, differentiate loca-
tion, timing, quality, intensity, and duration. Note if
radiation to the neck, axilla, or back is present.
c. Note location of murmur.
i. Aortic: second right intercostal space (ICS) next
to the sternum.
ii. Pulmonic: second left ICS next to sternum.
iii. Tricuspid: fth left ICS next to sternum.
iv. Mitral: fth left ICS at midclavicular line.
d. If murmur is heard, have the client squat, stand,
and/or perform the Valsalva maneuver. Squatting will
increase the blood to the heart and increase the left ventricular (LV) blood volume and stroke volume, which
will increase the sound of the murmur. Standing and the
Valsalva maneuver will provide the opposite, in which
the venous return will drop and reduce the ventricle size
and stroke volume and soften the sound of the murmur.
e. If the sound of the murmur occurs during the opposite
action, becoming softer when squatting and louder when
standing or during the Valsalva maneuver, consider
hypertrophic cardiomyopathy or MVP as the diagnosis.
2. Assess the neck and axilla for radiation.
DIAGNOSTIC TESTS
A. EKG.
B. Echocardiogram.
C. Chest radiography.
DIFFERENTIAL DIAGNOSES
A. Major differentiation should be in the description of mur-
mur as this aids in the identication of the murmur.
1. Timing:
a. Identify when the murmur occurs in the cardiac
cycle.
b. Systolic murmurs may or may not be normal.
i. Occurs between the S1“lub” and the S2“dub.”
c. Diastolic murmurs are always abnormal and need
further evaluation:
i. Occurs between the S2“dub” and the S1“lub.”
2. Quality: Is the sound harsh, blowing, musical, rum-
bling, vibratory, or soft?
3. Intensity: Murmurs are usually graded on a 6-point
scale:
a. Grade I: barely audible.
b. Grade II: audible but soft.
c. Grade III: easily audible without thrill.
d. Grade IV: easily audible, thrill usually palpable.
e. Grade V: audible with only the rim of the stetho-
scope on the chest wall; thrill present.
f. Grade VI: audible with the stethoscope barely off
the chest wall; thrill present.
4. Duration: Identify location and timing in the specic
phase of the cardiac cycle:
a. Holosystolic: throughout systole.
b. Holodiastolic: throughout diastole.
c. Midsystolic: midway between S1and S3.
d. Middiastolic: midway between S2and S1.
e. Decrescendo: starts loud at the beginning, then
tapers off.
f. Crescendo: starts soft at the beginning, then gets
louder.
5. Radiation: Murmur can be heard in another place, such
as the neck, back, left axilla, or across precordium. Sound
usually radiates in the direction of blood ow.
6. Location: Identify location on chest wall where mur-
mur is heard the best. Identify site: apex, pulmonary area,
tricuspid, and aortic areas. Radiation murmur may also
include axilla, left fourth ICS, or base of heart.
7. Conguration: Assess the intensity of the murmur
over time. Does it plateau, crescendo, decrescendo, or
crescendo–decrescendo?
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8. Systolic murmurs: Systolic murmurs are benign or
pathologic.
a. Early systolic murmurs:
i. Mitral regurgitation: Holosystolic; blowing
may be loud; located at fth ICS and radiates to left
axilla/back; heard best in the left lateral position
and with sudden squatting; intensity decreases with
the Valsalva maneuver and standing.
ii. Tricuspid regurgitation: Holosystolic; heard in
left lower sternal border or apex when right ventricle is enlarged; intensity increases with inspiration
and decreases with expiration; straight-leg raises
may increase intensity; may also see hepatojugular
reux.
iii. Physiologic: Early to midsystolic, low-pitch
normal S1–S2, located at left lower sternal edge at
third to fourth ICS; heard best with bell and supine;
disappears when sitting up or holding breath; commonly seen in children, pregnancy, and infection.
b. Midsystolic to late systolic murmurs:
i. Aortic stenosis: loud, hard crescendo–decre-
scendo at second-right ICS that radiates to the neck;
heard best when client is leaning forward; increases
with leg raise and lying at; decreases with Valsalva
and handgrip standing.
ii. Pulmonic stenosis: prolonged, loud S2 or cre-
scendo–decrescendo, usually greater than 3/6 at
second ICS and radiates to neck; increases with
inspiration.
iii. Hypertrophic cardiomyopathy (aortic outow
obstruction): peaks at midsystole; loud, harsh tone
at the left, lower sternal border that may radiate to
neck; increases with Valsalva maneuver and standing, decreases with sudden squatting; note brisk
carotid upstroke.
c. Late systolic murmurs:
i. MVP: midsystolic click heard before late sys-
tolic murmur, heard best at fth left ICS; heard best
with diaphragm; sitting or squatting may increase
intensity.
ii. Tricuspid valve prolapse: heard over the left
lower sternal border; delayed onset of murmur with
inspiration secondary to an increase in the right
ventricular volume.
9. Diastolic murmurs: Murmurs are always pathologic.
a. Early diastolic murmur:
i. Aortic regurgitation: high-pitch faint, decre-
scendo may start with S2, at third left ICS and radiate
down the sternal edge; heard best when the client is
leaning forward, holding breath; increases with sudden squatting or handgrip; may hear displaced point
of maximal impulse, S3, bounding pulse.
ii. Pulmonary regurgitation: valvular, dilation of
the valve annulus, congenital defect (tetralogy of
Fallot, VSD), and pulmonic stenosis; best heard over
the second/third left ICS; may be a high-pitched,
“blowing” sound in clients withhypertension; may
be pansystolic, having decrescendo conguration.
b. Middiastolic murmur:
i. Mitral stenosis: rumbling extends beyond mid-
diastole at fth ICS; heard best using the bell of the
stethoscope; increases with left lateral position; may
hear snap after S2.
ii. Tricuspid stenosis: increased ow across the tri-
cuspid valve, heard best at the left sternal border;
identied by its increase in intensity of the murmur
with inspiration (Carvallo sign); commonly seen
with mitral stenosis.
PLAN
A. General interventions:
1. Major therapeutic goals are to preserve quality of life,
increase life expectancy and exercise capacity, and reduce
risk of complications.
2. Activity restriction is not necessary in clients with
asymptomatic valvular disease.
B. Client teaching:
1. Reassure the client regarding specic diagnosis.
2. Counsel the client regarding their specic condition.
Teach the client signs and symptoms to report to the health
provider, including chest pain, SOB, difculty breathing,
and so forth.
C. Medical and surgical management:
1. Clients who need progressive increases in medications
to control symptoms may be candidates for valve replacement surgery.
D. Pharmaceutical therapy:
1. The 2017 focused update of the American Heart
Association (AHA) guideline does not recommend routine endocarditis antimicrobial prophylaxis treatment for
common valvular lesions, which include bicuspid aortic
valve, acquired aortic or mitral valve disease (including
MVP with regurgitation), and hypertrophic cardiomyopathy with latent or resting obstruction.
2. The European Society of Cardiology (ESC) published a
guideline in 2015 which continued to support the recommendations from the AHA 2007 guideline.
3. Endocarditis prophylaxis treatment: cardiac conditions:
a. It is recommended that clients with high-risk car-
diac condition abnormalities receive prophylactic
treatment. Specic cardiac conditions are as follows:
i. Prosthetic cardiac valves, including
transcatheter-implanted prostheses and homografts
or prosthetic material used for cardiac valve repair,
such as annuloplasty rings and cords.
ii. Previous infective endocarditis.
iii. Certain congenital heart diseases, such as cyanotic
congenital heart disease that has not been repaired; a
congenital heart disease that has been repaired with an
articial material or device for 6 months after repair;
and repaired congenital heart defects with continued
problems, such as leaks or insufcient ow at the prosthetic device or adjacent to the repair.
iv. Postcardiac transplant valvulopathy.
b. Procedures for high-risk clients mentioned earlier
that require prophylaxis treatment:
i. All dental procedures that involve manipula-
tion of the gingival tissue or the periapical region of
the teeth or perforation of oral mucosa.
ii. Incision or biopsy of respiratory mucosa or any
invasive procedure of the respiratory tract system.
iii. Procedures that include infected skin or muscu-
loskeletal tissue.
iv. Preventive treatment with antibiotics is not rec-
ommended for procedures that include the reproductive tract, urinary tract, or gastrointestinal tract.
c. Antibiotic prophylactic regimens include a single
dose 30 to 60 minutes before procedure:
i. Amoxicillin single dose: 2 g PO, intramuscular (IM),
or intravenous (IV) for adults or 50mg/kg for children.
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ii. Ampicillin 2 g IM or intravenous (IV) or 50mg/
kg IM or IV.
iii. Allergy to penicillin (PCN): cephalexin 2 g PO
for adults or 50mg/kg for children.
iv. Azithromycin or clarithromycin 500 g for adults
or 15mg/kg for children.
v. Allergic to azithromycin or clarithromycin:
Consider cefazolin or ceftriaxone 1 g IM or IV
for adults or 50 mg/kg IM or IV for children, or
clindamycin 600mg IM or IV for adults or 20mg/
kg IM or IV children.
d. Other pharmaceutical treatments depend on the
specic valvular abnormality:
i. Mitral stenosis: The mitral valve has a narrowing
that does not allow adequate blood to enter the LV
during diastole, usually because of rheumatic heart
disease. Mitral heart disease is the most commonly
seen valve effect with rheumatic heart disease.
ii. Diuretics, such as furosemide (Lasix) or hydro-
chlorothiazide (HydroDiuril), are used to control
edema.
iii. Digoxin (Lanoxin) or beta-blockers are used to
control atrial brillation (AF) and irregular heart rate.
iv. Warfarin (Coumadin) and the antiplatelet agent
aspirin (Bayer) are used to prevent clotting.
v. MVP: Echocardiogram is the recommended test
for the diagnosis of MVP. Usually no medications
are recommended except when clients are symptomatic or meet EKG requirements within current
cardiology guidelines.
1) Beta-blockers (such as Atenolol) may be
used for palpitations.
2) Diuretics should be avoided in clients who
are volume-reserved.
3) Oral contraceptives should be avoided in
females who exhibit neurologic symptoms.
vi. Mitral regurgitation: diuretics, digitalis, and
afterload-reducing agents for congestive heart failure (CHF):
1) Used in clients with aortic stenosis.
2) Diuretics are used for CHF.
3) Avoid vasodilators; they may result in pro-
found, irreversible hypotension.
4) Echocardiograms should be performed
every 6 to 12 months to follow the progression
of narrowing of the LV across the aortic valve.
vii. Aortic regurgitation: Afterload-reducing agents,
digitalis, and diuretics are recommended.
FOLLOW-UP
A. Most clients with valvular disease should be evaluated at
least once a year.
B. Clients on oral anticoagulation drugs need monthly
follow-up or as-needed prothrombin time/international normalized ratio if on warfarin.
CONSULTATION/REFERRAL
A. Consult a physician if the client is diagnosed with a new
murmur or exercise-induced symptoms during a sports physical examination.
B. Refer clients with newly diagnosed murmurs to a cardi-
ologist after obtaining echocardiogram results. Drug therapy
should be initiated according to diagnosis and symptoms.
C. Onset of AF with rapid ventricular response is an indica-
tion for immediate hospitalization.
D. Refer clients with systemic embolization to a physician for
emergent anticoagulation therapy and chronic oral anticoagulant therapy. Discuss the possibility of valve replacement with
a cardiologist.
E. If a new murmur is diagnosed in a pregnant client with a his-
tory of cardiac disease, refer them to a physician immediately.
F. All diastolic murmurs in pediatric clients indicate pathol-
ogy and need to be evaluated by a physician.
INDIVIDUAL CONSIDERATIONS
A. Pregnancy:
1. The development of a new, “high-ow” murmur in a
healthy female is not uncommon because of physiologic
changes occurring during pregnancy.
B. Pediatrics:
1. Perform a thorough cardiac examination on clients
from the time they are newborns through adolescence, so
that if a murmur is detected it can be compared.
C. Geriatrics:
1. A systolic murmur heard best in the aortic area may
indicate aortic sclerosis due to aging of the aortic valve
rather than true aortic stenosis.
BIBLIOGRAPHY
American Heart Association. (2019). Infective endocarditis. https://www.h
eart.org/en/health-topics/infective-endocarditis
Brusch, J. (2019, January 3). Infective endocarditis. Medscape. https://emedi
cine.medscape.com/article/216650-overview
Otto, C., & Nishimura, R. (2021). ACC/AHA Guideline for the Management
of Patients With Valvular Heart Disease A Report of the American College
of Cardiology/American Heart Association Joint Committee on Clinical
Practice Guidelines Developed in collaboration with and endorsed
by the American Association for Thoracic Surgery. American Society
of Echocardiography, Society for Cardiovascular Angiography and
Interventions, Society of Cardiovascular Anesthesiologists, and Society of
Thoracic Surgeons. Journal of the American College of Cardiology, 77, e25–197.
PALPITATIONS
DEFINITION
A. Palpitations are a feeling or an unpleasant awareness of
the heartbeat in the chest. They may be described as feeling a
sensation of the heart “ip-opping” or feeling a “rapid utter” of the heart.
INCIDENCE
A. The incidence of palpitations may range from 1% to 8% of
clients in a general practice setting.
PATHOGENESIS
A. Palpitations may be caused by the following:
1. Increase in stroke volume or contractility.
2. Sudden change in heart rate or rhythm.
3. Unusual cardiac movement within the thorax.
4. Hyperkinetic states, which cause constant pounding;
hyperthyroidism; and late-stage pregnancy.
5. Valvular heart disease that produces large stroke volumes.
6. Catecholamine release during anxiety or panic attacks.
PREDISPOSING FACTORS
A. Cardiac defects.
B. Severe anemia.
C. Hyperthyroidism.
D. Pregnancy.
E. Fever.
F. Anxiety.
G. Stimulants such as caffeine and certain drugs.
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