Exam 2: Cardiovascular Disorders

Cardiovascular Anatomy and Physiology

✦ Blood pressure in the artery is higher in the vein
✦ CO= stroke volume (SV) x heart rate (HR) (L/min). 46 L/min to pump the blood out
✦ SV is influenced by preload, after load, and contractility
✦ Metabolic demand is increase, vasodilation increased (increased O2)
✦ Systolic: the myocardial contraction and diastolic: when the muscle is relaxed
✦ preload: not a lot of blood go to ventricle, the preload will not be high, the right side collect
venous blood
✦ contractility: the force of contraction, thing that medication can contractility, check heart rate
when giving digoxin

Cardiovascular Assessment
✦ Cardiovascular disease is the leading disease in women
✦ Cardiovascular health problem complaints: chest pain, acute coronary syndrome (SOB, dizziness, back
pain, abdominal pain ,nausea, sweating, jaw pain), cardiac arrest, weight gain, edema (heart
failure patient). Injection fraction???- diagnostic identify heart failure. Normal injection
fraction is 50-70%
✦ Assessment parameters: most pt delayed treatment (don’t go the doctor, disregard the symptoms).
have to look at family history, what medications are they taking, assess nutrition, diet, and
metabolism, do they have trouble bowel movement, vagal???, do they go the doctor routine?, do they
have cardiologist, do they know the risk factors (non modified and modified), do they exercise
(physical activity), cognition, decrease sexual drive, do they have successful coping mechanism,
stress level, do pain assessment
✦ Physical assessment: look at their skin (skin assessment, palpate and assess it), get their height
and weight, get their BP, do they have osthostatis hypotension, check cap refill, check their pulse
(DP, femoral, TB, brachial, radial, ulnar), assesses the rate and rhythm (is it weak, fast,
bounding) of the pulse, inspect the jugular vein, 6Ps- pain, pallor, paresthesia, paralysis,
pulselessness, poikilothermic. Listen to heart sound (S1 and S2), S3 and S4 are abnormal; friction
rub- result of inflammation, grating sound
✦ Diagnostic studies: cardiac biomarker, CK-MB, hemoglobin is elevated in the first 24 hrs and then
return to normal, cholesterol level LDL less than 160, HDL 35-85, BMP 100-300 indicate the client
have heart failure, EKG/ECG, stress test, echocardiogram (ultra sound), nuclear stress test????,
hemodynamic monitoring- risk for pneumothorax, infection , pulmonary embolism????, CT angiogram.
General rule of thumb: no caffeine or any types of stimulants (chocolate) for 4 hrs if they are
having stress test and CT angiogram. But they can take cardiac meds with a small sip of water. They
need to be monitor 15-20 mins after we send them home. Allen test. ABI test. TEE test (make sure
gag reflex return).
Hypertension (120/80)- known diagnosis
✦ Introduction:
- About 78 million American adults in the U.S. have HTN. Another 1 in 3 American adults has
prehypertension (BP higher than normal 120/80 or lower but not yet in the high BP range)
- Asymptomatic and must be measured to be detected, “silent killer”
- Undiagnosed, untreated, or underrated HTN may lead to target organ damage causing myocardial
infarction (MI), kidney damage or failure, cerebrovascular accident (CVA), or hypertensive
retinopathy
- High BP was a primary or contributing cause of death for more than 360,000 Americans in 2013
- Over the past decade, BP control increase by 55% among adults aged 18 yrs and above

✦ Hypertension:
- Normal: BP of less than 120/80 mmHg diastolic
- Prehypertension: BP of 120-139/80-89 mmHg
- HTN: BP of 140/90 mmHg or higher

- Diagnosis for hypertension based on those under 60 yrs of age and those over 60 yrs of age
- All individuals who have diabetes and/or chronic kidney disease (CKD) should receive treatment
to keep the BP below 140/90
- HTN is classified as stage 1 or 2 depending on its severity
• Stage 1: systolic pressure is 140-159 mmHg or greater and/or the diastolic pressure is
90-99 mmHg
• Stage 2: systolic pressure is 160 mmHg or higher, or the diastolic pressure is 100 mmHg or
higher
• Severe HTN is demonstrated w/the systolic BP greater than or equal to 180 mmHg or the
diastolic BP greater than or equals to 110 mmHg
- The term resistant HTN is used to define pt whose conventional BP remains uncontrolled by 3
cases of antihypertensive agents, including diuretic. The term refractory and resistant are
used interchangeably
- Diagnosis of HTN should be based on the average of 2 or more accurate BP measurements taken
during 2 or more contacts with a health care provider
- BP should measured accurately in both arms, using the higher reading, palpate the brachial
pulse prior to measurement and use the correct cuff size
- The pt should seated for at least 5 mins; smoking and eating should be avoided for 30 mins, the
arm should be at heart level

✦ Pathophysiology:
- BP is the product of cardiac output (CO) x peripheral vascular resistance (PVR)
- CO: the volume of blood being pumped by the heart per min and is the product of HR x SV (the
amt of blood pumped out from the ventricles per beat)
- PVR is R/T the diameter of the blood vessel and the viscosity of the blood
• The thicker the blood or smaller the radius of the blood vessel, the higher the resistance
• The thinner the blood or larger the diameter of the blood vessel, the lower the PVR
- For HTN to develop, there must be a change in one or more factors affecting PVR or CO
- Management of HTN: decrease peripheral resistance or blood volume, or strength, force, and rate
of myocardial contraction
- BP tend to be highest shortly after awakening and then decrease throughout the day, reaching
the lowest point btwn 2 and 5 am (known as dippers)
- Those who reflect a pattern of a flattened 24-hr BP profile are referred as nondippers
• Higher risk for cardiovascular and kidney disease

- Primary HTN (90-95% out of 100% HTN cases ):

• High BP from an unidentified cause
• Essential or idiopathic HTN
- Secondary HTN:
• High BP R/T identified cause
• Causes: narrowing of the renal arteries or renal artery stenosis, kidney disease,
hyperaldosteronism (mineralocorticoid HTN), medications, pregnancy, and coarctation of the
aorta
- White-coat HTN:
• Normal ambulatory BP readings but elevated pressure (> 140/90 mmHg) in a health care clinic
• Should have follow-up with ambulatory home BP monitoring to determine if the situation is
isolated
• Ambulatory monitoring determine if masked HTN exists and if systolic HTN is present, it
will help to prevent overdiagnosis and treatment, which may cause unnecessary side effects
• An increased risk of developing systolic HTN
 • These clients need to receive active follow-up and lifestyle counseling
• Elevations in BP w/o tachycardia or complaints of pain, can be predictive of developing HTN
later in life
- Masked HTN:
• Present as normal pressure reading in provider settings but elevated BPs at home or work
• Known to be a precursor of sustained HTN
• High as 70% in African Americans
• R/T daily stressors at work, smoking or alcohol use, oral contraceptive use, and sedentary
habits
• Suspected in men, those w/diabetes or kidney disease, those w/transiently elevated BP,
those appear with normal/high-normal daytime ABPM of 130-135/80-85 mmHg, those w/
obstructive sleep apnea and autonomic dysfunction
• An increase prevalence of metabolic risk factors, left ventricbucler hypertrophy, carotid
plague, demonstrating the impact of HTN on organ fxn
• At particular risk for CVD b/c of delays in diagnosis and Tx
• When the at-risk individual is identified, the nurse advocates for the use of home BP
monitoring to confirm the diagnosis and monitor treatment

✦ Risk factors:
- Associated factors for essential HTN: heredity, obesity, sleep apnea, advancing age, renal
changes, ethnicity/race
- Possible factors: diabetes, type A personality, smoking, sedentary lifestyle, hypothyroidism
- Poor diet. A diet high in Na+ and low in K+ may contribute to HTN especially in those who are
sodium sensitive. About 5% of individuals have Na+ sensitivity that can affect their BP
- Factors contributing to HTN may include increased sympathetic nervous system activity &
increased renal absorption of Na+, Cl-, and H2O
- Other contributing factor: increased activity of the renin-angiostensin-aldosterone system,
causing expansion of extracellular fluid volume and increased SVR, or dysfunction of the
vascular endothelium
- Resistance to insulin may be a common factor linking HTN, type 2 diabetes mellitus,
hypertriglycerdemia, obesity, glucose intolerance
- The prevalence of HTN increase with aging (systolic pressure rise throughout life, diastolic
pressure rise until 50 yrs old)
• Those who are normotensive at age 55 have a 90% lifetime risk for developing HTN
• Before age 45, men are more likely to have HTN than women
• When women reach menopause, loss of hormonal protection occurs, risk for HTN rises
• After age 64, HTN are more likely to affect women
• Men younger than 55 are more likely to have uncontrolled HTN than women
• After age 65, women are more likely to have uncontrolled high BP
• Black males, Mexican-American males, and younger adults age 20-39 have a higher likelihood
of uncontrolled BP
- HTN can affect anyone
• More common in African-Americans adults than in Caucasian adults
• African-Americans have an earlier onset, higher prevalence, and a greater rate of stage 2
HTN, leading to higher incidences of nonfatal stroke, death from heart disease, & end-stage
kidney disease
Are less likely than Caucasians to achieve target control level with treatments (mostly
in male, overweight or obese, physically inactive, smokes, diabetes)

- Systolic HTN is the most common form of HTN and is a major risk factor for CVD. As the “baby
boomers” generation ages, its incidence is expected to increase
- Obesity is one of the common risk factors for developing HTN
- HTN, a risk factor for atherosclerotic heart disease, often coexists with dyslipidemia,
diabetes mellitus, and a sedentary lifestyle
- Metabolic syndrome or syndrome X occurs when 3 of the following symptoms are present
simultaneously:
• BP elevation greater than 130/85
• insulin resistance
• dyslipidemia
• abdominal obesity
- Metabolic syndrome place the pt at risk for CVD and diabetes. The risk for CVD doubles with
each increment of 20/10 mmHg above 115/75 mmHg
- Oral contraceptive use (birth control pills) causes a small increase in systolic and diastolic
BP, when accompanied by smoking and obesity, results in HTN 3 times more than those w/o risk
factor
 • Use of oral contraceptive is the most common cause of secondary HTN in women. Question
female clients regarding medication use
- Cigarette smoking does not cause high BP. However, if a person with HTN smokes, his/her risk of
dying from heart disease or related disorders increases significantly

Risk factors for cardiovascular problems in hypertensive patients:

Major risk factors (in addition to HTN)
- Smoking
- Dyslipidemia (elevated LDL or total cholesterol and/or low HDL cholesterol)
- Diabetes mellitus
- Impaired renal function (GFR less than 60 mL/min and/or microalbuminuria)
- Obesity (BMI of 30 kg/m2 or higher)
- Physical inactivity
- Age (over 55 years for men, 65 years for women)
- Alcohol use
- Family history of CVD (in female relative under 65 yrs of male relative under 55 yrs)

Target organ damage or clinical CVD

- Heart disease (left ventricular hypertrophy, angina, or previous MI, previous coronary
revascularization, heart failure)
- Stroke (cerebrovascualr accident, brain attack) or TIA
- Chronic kidney disease
- Peripheral arterial disease
- Retinopathy

✦ Gerontologic considerations:
- Half of individuals aged 60-699 and 75% of individuals over age 70 are affected
- Aging causes structural and functional changes in the heart and blood vessels, including
atherosclerosis & decreased elasticity of the major blood vessels
- Because of increased wall stiffness, the arteries are less able to buffer the pressure created
as blood is ejected from the left ventricle and unable to store the energy to exert diastolic
pressure
- More likely to suffer form the complication of HTN and are more likely to have uncontrolled
disease
- Isolated systolic HTN w/widened pulse pressure is more common in older adults, associated with
cardiovascular and cerebrovascular morbidity and mortality, as well as dementia
- Elderly hypertensive pt have:
• lower CO, higher peripheral resistance
• wider pulse pressure
• lower intravascular volume
• lower renal blood flow

- The average elderly American is on more than 6 mediations, which put them at risk for
polypharmacy
- Not all medications are for high BP, but many interact with antihypertensive medications (i.e.
NSAIDS used for arthritis, can raise BP)
- The drug regimen of an elderly pt with HTN should be reviewed carefully at every visit
- An orthostatic decline in BP accompanies advanced age & contribute to an inevitable adverse
effect with some antihypertensive drugs
- Systolic BP lower than 130 and diastolic BP lower than 70 mmHg are best avoided in
octogenarians. An initial goal of less than 140/90 mmHg is reasonable in elderly pt, and
achieved systolic BP of 140-145 mmHg is acceptable in octogenarians
- Restricting Na+ sodium lower BP more in older adults than in younger adults
• In DASh trail, systolic BP decreased by 8.1 mmHg with sodium restriction in hypertensive pt
aged 55-76
• Thiazide diuretics should be used with caution b/c of risk of hyponatremia and volume
depletion
- Should begin Tx w/lifestyle modifications to decrease the risk of cardiovascular and
cerebrovascular
- If medications are needed to achieve BP goal, the starting dose should be half that used in
younger pt and increased slowly. “Start low and go slow”
- Compliance may be more difficult for the elderly when memory impairment exists or due to the
expense of treatment plans
 - Ensure the patient understands the regimen & can see and read instructions, open the med
container, and get the prescription refilled
- Encourage adherence to the treatment plan, and know when and whom to call for questions or
problems
- Nursing alert: The elderly are more sensitive to volume depletion cause by diuretics and to
sympathetic inhibition caused by adrenergic antagonists. Educate the pt to change position
slowly when moving from lying or sitting position to a standing position and to use supportive
devices to prevent falls that could result from dizziness

✦ Clinical manifestations and assessment:

- Monitor BP. Ensure proper BP measurement technique is being used (review box 13-1) and
manometers used are calibrated (the nurse should select a cuff w/length of 80% of arm
circumference, and width of about 40% of arm circumference)
- To avoid undermeasurement of the SBP with auscultatory gap, the nurse should inflate the cuff
to palpate the brachial artery until the pulse is obliterated, deflate the cuff, add 30 mmHg to
the palpated pressure, and auscultate the BP and record results
- Automated BP measurement devices are less accurate than are trained observers using the
auscultatory method. It’s recommended their use to be limited to when frequency and less
accurate methods of BP assessment are needed. Providers should auscultate BP to diagnose and/or
evaluate the management HTN

- Pt may report early morning headaches, dull aching headache throughout the day, visual
disturbances (difficulty with their vision), orthostatic HTN or hypotension, fatigue, and
proteinuria, elevate BP
• Nursing alert: Normally, BP should vary by no more than 5 mmHg btwn arms. If there is a
difference, record both initially. Later, record the higher number. A difference of 10 mmHg
or more btwn the pt’s arms may indicate thoracic outlet syndrome or arterial obstruction on
the side with lower value
- Many symptoms associated with target or end-organ damage. The nurse should ask the pt about
anginal pain; SOB; alterations in speech, vision, or balance; epistaxis (nose bleed);
headaches; dizziness; nocturia
- Further assessment include asking about personal, social, or financial factors, or unacceptable
pharmaceutical side effects that may interfere with the pt’s ability to adhere to the med
regimen
- Asymptomatic, but when S/S appear, vascular damage R/T organs served by the involved vessel has
occurred
- Focus on cardiovascular assessment. Coronary artery disease with angina or MU is a common
consequence of HTN
• Left ventricular hypertrophy occurs in response to the increased workload placed on the
ventricle as it contracts against higher systemic pressure
• When heart damage is extensive, HF follows (90% of the time), HTN preceded CHF
• Pathologic changes in the kidneys indicates by microalbuminuria, increased blood urea
nitrogen (BUN) and serum creatinine levels, and nocturia result
• Cerebrovascular involvement lead to stroke or transient ischemic attack , manifested by
alteration in vision os speech, dizziness, weakness, a sudden fall, or hemiplegia
• Retinal changes such as hemorrhages, exudates (fluid accumulation), arteriolar narrowing,
and cotton-wool spots (small infarctions) occur
• In severe HTN, papilledema (swelling of the optic disc) may be seen
• A risk factor assessment is need to classify and guide the Tx of the hypertensive
individual at risk for cardiovascular damage

- Routine lab test evaluate for rand-organ damage, which include:

• urinalysis
• evaluation for microalbuminuria or proteinuria
• blood chemistry (i.e. analysis of Na+, K+, BUN, & creatinine, fasting glucose, and total
and HDL cholesterol levels)
• 12-lead electrocardiogram (ECG)
• Additional studies include: creatinine clearance, renin level, urine tests, and 24-hr urine
protein
• The eyes should be assessed for hypertensive retinopathy
• Look at urine, fat and glucose, cholesterol, lactic build up in the vein which cause narrow
vessel, renal failure

✦ Medical and nursing management:

- Maintain a BP of less than 140/90 mmHg is the goal for treatment
- The aim for individuals with prehypertension and no complicating conditions is to lower BP to
normal
- To prevent or delay progression to HTN, encourage ppl with BPs in the prehypertension category
to ebbing lifestyle modifications (i.e. dietary changes and exercises)
- JNC8 recommends that ppl over the age of 60 begin pharmacologic Tx when the BP id greater than
150/90, lifestyle changes should be emphasized
- PCP should monitor these pt every 1-3 months until their BP goal is reached and then 3-6 months
thereafter
- Those with diabetes or CKD should attain a target pressure of less than 130/80 mmHg
- The clinician uses the Tx algorithm, rick factor assessment data, and the pt’s BP category to
choose Tx plans for the pt
- The nurse encourages self management, including self BP monitoring and educate to initiate and
maintain lifestyle changes. It’s important to assess the pt’s beliefs about HTN
- Self management and education empowers pt to ask questions and voice concerns, these
individuals are less likely to be hospitalized, fewer emergency department and unscheduled
medical visits, and fewer days off from work
- The nurse should routinely ask whether its take herbal supplements or OTC meds that may
increase BP (including caffeine and ephedra- stimulants; licorice, which has an aldosterone-;ke
effect; oral contraceptives, acetaminophen and NSAIDs which may lead to fluid retention
- Certain agents have been touted as BP-lowering agents (i.e. coenzyme Q10, garlic, vit C, and L-
arginine
- Pt should be cautioned that nutritional supplements are not regulated in the same manner as
pharmaceuticals, and all products used should be reported to the PCP

- Lifestyle changes:
• Weight loss, reduces alcohol and sodium intake, smoking cessation, and regular physical
activity for 30 mins on most days are effective lifestyle adaptations to reduce BP.
• Treatment of sleep apnea, underlying thyroid disorder, and management of blood glucose are
recommended
• The nurse should emphasize the concept of lifelong BP control and adherence to Tx rather
than cure and absolute compliance
• Offer info regarding lifestyle modifications to reduce BP
• Adhering to DASH approach helps decrease BP and lower lipid levels, reducing the risk of
CVD
DASH is low in saturated and trans fat as well as rich in K+, Ca2+, Mg2+, fiber, and
protein
Emphasizes vegetable, fruits and fat free or low fat diary produces (i.e. whole grain,
fish, poultry, beans, seeds, nuts and vegetable oils) and limit sodium, sweets, surgery
beverages and red meat which lower BP and prevent CVD
The average daily sodium intake for Americans age 2 yrs and older is 3,400 mg. With
DASH approach, the target sodium intake should be 2,300-2,400 mg daily
Those with HTN, diabetes, CKD, Africa American, individual older than 51 should reduce
sodium intake to 1,500 mg daily
About 5% of pt have sodium-sensitive HTN and should be cautions with sodium intake
(i.e. elderly)
A diet high in fruits and vegetables is associated with lower systolic and diastolic BP
• Maintain a normal weight. Obesity may increase the risk of HTN through overactivation of
the sympathetic nervous system, activation of renin-angiotensin-aldosterone system, sodium
retention and increase HR
• The impaired production of nitric oxide, a potent vasodilator, impairs vasodilation and
causes an increased resting BP
• Regular exercise is associated with lower BP regardless of BMI, improve inflammatory
markers and cause an increase in endothelial nitric oxide synthase, a potent vasodilator
• Achieve a waste circumference of less than 40 in for men and less than 35 for when and a
BMI btwn 18.5 and 24.9 kg/m2
• A weight loss of only 10 lb may result in 5 to 20 mmHg reduction in SBP, offering tangible
results tot the pt
• Nursing alert: reducing table salt to about 1 teaspoon per day, 2.3 to 2.4 g of sodium, can
reduce systolic BP by 2-8 mmHg

- Alternate therapies:
• Complementary, alternative medicine therapies, mind-body interventions reduces BP (i.e.
relaxation, meditation, guided imagery, hypnosis, biofeedback, yoga, Tai Chi)
• Physical activity and exercise reduce morbidity and mortality for coronary heart disease,
HTN, obesity, diabetes, and osteoporosis. Also have positive effect on the pt’s
psychological well-being
 - Blood pressure monitoring:
• Ensure that follow-up is provided for any person identified as having an elevated BP level
• Each person should be given a written record of his/her BP at the screening
• Reductions in BP are greater when pt are partners and participate in self-management,
including diaries and technology-based applications

- Pharmacologic therapy:
• African American men with depressive symptoms, psychological stressors, and substance abuse
as a population at high risk for non adherence to treatment
• In the general population, include diabetes but exclude African Americans, initial
antihypertensive treatment should include:
Thiazide-like diuretic: are useful in elderly and in pt w/osteoporosis b/c they
decrease bone breakdown and preserve bone integrity
Calcium-channel blocker (CCB): such as amlodipine, exert their major effect on blood
vessel and are recommended for the Tx of HTN, while meds (diltiazem) that affect HR are
better suited to rhythm control
Angiotensin-converting enzyme inhibitor (ACEI): protect and preserve kidney fxn and
protect the vascular endothelium
Angiotensin-receptor blocker (ARB): protect and preserve kidney fxn and protect the
vascular endothelium
• In African American population, Tx include thiazide and CCB
• The main objective of HTN Tx is to attain & maintain goal BP:
If the goal is not attained within 1 month of Tx, increasing the dose of the 1st drug
or adding a second drug from one of the classes was recommended
The advantage of adding a med, is that side effects may be avoided
Most pt requiring pharmacologic intervention need 2 meds for effective Tx as HTN is
caused by multiple factors
• ACEI and ARB are not recommended for use at the same time
• A recommendation against use of beta-blockers for the initial Tx of HTN. A higher rate of
cardiovascular death, MI, or stroke when compared to use of an ARB

Lifestyle changes:
-Smoking cessation
-Control blood glucose lipids
-Weight loss
-Diet:
• Eat healthy (i.e. DASH diet)
• Moderate alcohol consumption, reduce alcohol intake
• Reduce sodium intake to no more than 2,400 mg/day
-Physical activity
• Moderate to vigorous activity 3-4 days a week averaging 40 per session

- Table 13.4 (Med therapy for HTN)

✦ Hypertensive crisis:
- Hypertensive crisis: a diastolic BP of higher than 180/120 mmHg (1% of HTN individuals have
it). Occur when HTN is untreated or poorly controlled as well as in those discontinued their
meds
- Common in men, older adults, African Americans
- Causes: head injury, pheochromocytoma (a tumor of the adrenal medulla that causes excess
secretion of catecholamines), food-drug interaction (i.e. tyramine combined with a monamine
oxidase [MAO] inhibitors), eclampsia or preeclampsia, substance abuse (i.e. cocaine
intoxication), and kidney disease
- Once the crisis is managed, the nurse strategizes with the pt and provider to control of his/
her BP and prevent recurrence

- Two classes of hypertensive crisis that require immediate intervention: hypertensive emergency
and hypertensive urgency
• Hypertensive emergency:
A situation in which diastolic BP is greater than 120 mmHg and must be lowered quickly
to halt or prevent damage to the target organs
Conditions associated w/hypertensive emergency include eclampsia or preeclampsia, MI,
dissecting aortic aneurysm, intracranial hemorrhage, hyperthyroidism or thyroid storm
 Pt present with severe elevations in BP, accompanied by rapidly progressive target
organ dysfunction (i.e. myocardial or cerebral ischemia or infarction, pulmonary edema,
kidney failure)
Pt complaints include headaches, confusion, blurred vision, N/V, seizures, pulmonary
edema, oliguria, hypertensive retinopathy
The therapeutic goals are a controlled, gradual reduction of the BP by 10% in the 1st
hr and by an additional 15% during the next 3-12 hrs to a BP of no less than 160/110
mmHg
It is important not to become overeager and lower BP too quickly (cerebral
hypoperfusion may occur if the mean BP is lowered more than 40% in the initial 24 hrs),
b/c of hypoperfusion to the brain, heart, kidneys, and retina an MI or CVA could result
The exceptions include aortic dissection and postoperative bleeding from the vascular
suture lines, in which a more rapid normalization of BP
A pt experiencing hypertensive emergency will receive care in the ICU with BP measured
every 5 mins while unstable
The nurses evaluates the pt for a precipitous drop in BP, requires immediate action to
restore BP and perfusion to normal levels

• Hypertensive urgency:
A situation in which BP is severely elevated, no evidence of impending or progressive
target organ damage
Elevated BPs associated with severe headache, epistaxis, anxiety are classified as
urgencies
Reducing BP can be accomplished by increasing the dose of the pt’s current meds or by
adding a second med
Oral med with rapid onset of action may be used, including clonidine (Catapres),
captopril (Capoten), or labetalol (Trandate). This can be accomplished by keeping the
pt in the ER department for several hrs, followed by outpatient assessment within 1 to
3 days

• Pharmacologic management of hypertensive crisis:

Meds of choice in hypertensive emergencies are best managed with continuous IV infusion
of short-acting titratable antihypertensive agent.
➡ Should avoids the sublingual and IM routes as their absorption and dynamics are
unpredictable. Meds include hydrochloride, sodium nitroprusside, mesylate, etc.
which have immediate, short-lived actions
➡ Nitroprusside should be used cautiously due to thiocyanate toxicity, erratic
responses, and risk for severe hypotension
Oral doses of fast-acting agents such as clonidine or labetalol are recommended of the
Tx of hypertensive urgencies
ACEIs and ARBs block aldosterone and may cause hyperkalemia when used with potassium-
sparing diuretics or salt substitutes that contain K+. The nurse should monitor the K+
level and teach the pt to avoid salt substitute

✦ A community health nurse is teaching a group of adults about hypertension. What is a risk factor
that the nurse should mention?
A. Cardiac dysrhythmias
B. Hyponatremia
C. Hyperkalemia
D. Dyslipidemia- abnormal cholesterol level

✦ Complications:
- Prolonged BP elevation damages blood vessel (i.e. heart, kidneys, brain, eyes)
- Prolonged uncontrolled HTN will lead to:
• Myocardial infarction
• Heart failure
• Left ventricular hypertrophy
• Renal/kidney failure
• Stroke
• Impaired vision
- An acute elevation BP associated with end-organ damaged is termed hypertensive crisis

✦ Hypertensive Crisis:
- Hypertensive emergency: situation in which BP is higher than 180/120 usually due to
hypertension of pregnancy, MI, dissecting aortic aneurysm, and intracranial hemorrhage. Goal
is reduce it by 25% in the first hour then goal pressure of 160/100 26 hrs
- Hypertensive urgency: BP is severely elevated but no evidence of impending of progressive
organ damage, associated symptoms (headache, epitaxis or anxiety)
Coronary Vascular Disorders
✦ Coronary Atheroclerosis
- Introduction:
• The most common cause of CVD in U.S. is atherosclerosis, an abnormal accumulation of lipid
or fatty substances and fibrous tissue in the lining of arterial blood vessel walls
• These substances create blockages and narrow the coronary vessels in a ways that reduces
blood flow to the myocardium
• Involves a repetitious inflammatory response to injury to the artery wall and subsequent
alteration in the structural and biochemical properties of the arterial walls

- Pathophysiology:
• Begins as fatty streaks of lipids deposited in the intimate of the arterial wall. These
lesions being early in life. Genetics and environmental factors influence the progression
of these lesions
• Continued development of atherosclerosis involves an inflammatory response, begins w/injury
to the vascular endothelium
The injury may be initiated by smoking, HTN , other factors
The presence of inflammation has multiple effects on the arterial wall, including the
attraction of inflammatory cells
• The macrophages infiltrate the injured vascular endothelium and ingest lipids, which turns
them into what are called “foam cells” (present in all stages of atherosclerotic plaque
formation)
• ==Activated macrophages release biochemical substances damage the endothelium, attracting
platelets and initiate clotting
• Smooth muscle cells within the vessel wall proliferate and form a fibrous cap over a center
the is filled with lipid and inflammatory infiltrate. These deposits, called atheroma or
plagues, protrude into he lumen of the vessel, narrowing it and obstructing blood flow
• If the fibrous cap of the plague is thick and the lipid pool remains relatively stable, it
can resit the stress from blood flow and vessel movement
• If the cap is thin and inflammation is ongoing, the lipid core may grow, causing it to
rupture, may cause thrombus formation
• Then the thrombus obstruct blood flow, leading to sudden cardiac death or an acute
myocardial infarction (MI), which is the death of a portion of the heart muscle
• Atherosclerosis can produce narrowing of the lumen of a blood vessel, sudden obstruction of
a blood vessel due to plague rupture, and weakening of a blood vessel, resulting in
aneurysm formation or emboli formation b/c of direct damage to the endothelium
• Vasospasm (sudden constriction or narrowing) of a coroner artery, myocardial trauma from
internal or external forces, structural disease, congenital anomalies, decreased O2 supply
(i.e. from acute blood loss, anemia, or low BP), and increased O2 demand (i.e. from rapid
HR, thyrotoxicosis or use of cocaine)

- Risk factors:
• Some risk factors are uncontrollable, including:
Age (men over 45 yrs old, women over 55 yrs old)
Gender (<55 men at risk, >55 women and men, women under 55 yrs of age who have
premature menopause w/o estrogen replacement therapy)
Race (African American, Mexican American, Native American, and some Asian American)
Family history of first-degree with premature diagnosis of heart disease
• Known modifiable risk factors:
Diabetes and pre diabetes
HTN, smoking, obesity
Physical inactivity, high blood cholesterol,
Unhealthy diet, and stress
• Other risk factors:
Sleep apnea, metabolic syndrome
Increased body mass index
Chronic kidney disease, chronic infections
Nonalcoholic fatty liver disease, influenza
Proinflammatory (i.e. rheumatoid arthiritis)

• A cluster of metabolic abnormalities now known as metabolic syndrome is known to be a major

risk factor for CAD. A diagnosis of this syndrome includes any combination of 3 of the
following conditions:
Insulin resistance (fasting glucose greater than 110 mg/dL or abnormal glucose
tolerance test)
 Abdominal obesity (waist conference greater than 35 inches in women, greater than 40
inches in man)
Dyslipidemia (triglycerides greater than 150 mg/dL); HDL less than 50 mg/dL in women,
less than 40 mg/dL in men)
HTN (at least 130/85 mmHg)
Pro-inflammatory state (high levels of C-reactive protein)
Prothrombotic state (high fibrinogen)
• Many people with type 2 diabetes mellitus fit this clinical picture. Measurement of
lipoprotein, homocysteine (an AA associated with cardiac disease), and CRP may also be
appropriate in ppl who are identified as being at risk

- Clinical manifestations:
• Produce symptoms and complications according to the location and degree of narrowing o the
arterial lumen, thrombus formation, and obstruction of blood flow to the myocardium.
• Usually progressive, causing an inadequate blood supply that deprives the cardiac muscle
cells of O2 needed for their survival. The condition known as ischemia
• Angina pectoris: chest pain that is brought about by myocardial ischemia
• If the decrease in blood supply is significant enough, of long enough duration or both,
death of myocardial cells, or MI, may result
• Irreversibly damaged myocardium undergoes degeneration and replaced by scar tissues causing
various degrees of myocardial function
• Significant myocardial damage may result in persistently low CO, and if the heart cannot
support the body’s needs for oxygenated blood, the result is heart failure
• Myocardial hypoxia due to CAD may also lead to lethal cardiac rhythms disturbance that may
result in sudden cardiac death
• Nursing alert: S/S of myocardial ischemia include acute onset of chest pain, SOB, extreme
fatigue, diaphoresis, N/V
• In elderly, they might have “silent” ischemia.
Encouraged to recognize their chest pain like symptom (angina equivalent), i.e.
weakness, as an indication that they should rest or take prescribed medication and
contact their PCP with concerns
Pharmacologic stress testing used to diagnose CAD CAD in elderly pt or those who have
limited ability to exercise b/c of other conditions (i.e. peripheral vascular disease,
arthritis, degenerative disk disease, physical disability, foot problem)

- Prevention and medical and nursing management:

• Controlling cholesterol abnormalities:
The metabolism of fats is an important contributor to the development of CAD. Fats
( insoluble in H2O) are encased in water-soluble lipoproteins that allow them to be
transported within the circulatory system
Four elements of fat metabolism: total cholesterol, LDL, HDL, and triglycerides which
affect the development of heart disease
Cholesterol is processed by the GI tract into lipoprotein globules (chylomicrons),
which reprocessed by the liver as lipoproteins. This is a physiologic process of the
formation of lipoprotein-based cell membranes and other important metabolic
processes.When excess LDL is produced, LDL adhere to vulnerable points in arterial
endothelium. Macrophages ingest them and leading to the formation of foam cells and the
beginning of plaque formation
Patients who have had an acute event (i.e. MI) a percutaneous coronary intervention or
coronary artery bypass graft require assessment of LDL cholesterol level b/c LDL levels
may be low immediately after the acute event of procedure. Lipids should monitors
regularly until the desired level is achieved
LDL exerts a harmful effect on coronary vasculature b/c it can transported easily into
the vessel lignin
HDL promotes the used of total cholesterol by transporting LDL to the liver where it
biodegraded and excreted. The lvl of HDL should exceed 40 mg/dL and ideally more than
60 mg/dL. High HDL lvl is a strong negative risk factor for heart dies (it protect
against disease)

The group who would benefit form statin therapy (cholesterol lowering meds) are those:
➡ With clinically evident atherosclerotic CVD
➡ With LDL cholesterol level of at least 190 mg/dL
➡ With type 1 or type 2 diabetes (age 40-75) and LDL level of 70 mg/dL or higher, w/o
evident atherosclerotic CVD
➡ W/o evident atherosclerotic CVD or diabetes with LDL cholesterol lvl range of 70-189
mg/dL and 10-year risk of atherosclerotic CVD of at least 7.5%
 Moderate-intensity statin therapy (aim for a reduction of 30% to less than 50% in LDL
cholesterol level) is recommend for pt who cannot tolerate high-intensity Tx or pt with
diabetes and a 10-year risk of atherosclerotic CVD of less than 7.5%. Ppl receive
statin therapy should monitor for muscle and hepatic injury and for new-onset diabetes

• Treating hyperlipidemia
Lipid-lowering med reduce CAD mortality in pt w/elevated lipid lvl and at-risk pt w/
normal lipid lvl
Pt with elevated cholesterol levels should be monitored for adherence to therapeutic
plan, the effect of cholesterol-lowering medications, and the development of side
effect
Lipid lvl are obtained and adjustments made to diet and med every 6 weeks until lipid
goal or max dose is achieved and then every 6 months after
Lifestyle changes need to be incorporated into nay tx regimen and include:
➡ Dietary measures include a heart- healthy diet
➡ Increase physical activity
➡ Smoking cessation
➡ stress management, HTN management, diabets management

• Managing HTN
The risk of CVD increase as BP increase. Elevated BP result in increased stiffness of
the vessel wall, lead to vessel injury and resulting inflammatory responses within
intima. Can cause vessel hypertrophy and hyperresponsiveness, resulting in acceleration
and aggravate of atherosclerosis. HTN increase the work of left ventricle, which mist
pump harder to eject blood into arteries. The increase workload causes the heart to
enlarge and thicken and lead to heart failure

• Controlling diabetes mellitus

Pt w/diabetes are 2-4 times more likely than nondiabetic pt to experience development
of CVD
Hyperglycemia fosters dyslipidemia, increased platelets aggregation, and altered RBC
fxn, can lead to thrombus formation
Effective tx with appropriate anti-hyperglycemic agents and diet has shown improvement
in endothelial function and improved endothelial-dependent dilation

✦ The nurse is caring for a patient who had a recent MI. The nurse is aware that the plague that
likely contributed to this event is mostly made up of which of the following?
A. Lipids???
B. Dead leukocytes
C. Interferons
D. Adipose tissue

✦ Angina pectoris
- Definition: A clinical syndrome characterized by episodes or paroxysms of pain, pressure, or
discomfort in the chest, jaw, shoulder, back, or arm that is caused by myocardial ischemia
• The cause is insufficient coronary blood flow (caused boy atherosclerotic disease),
resulting in a decreased O2 supply when increased myocardial demand for O2 in response to
physical exertion or emotional stress
• The demand for O2 exceeds the supply
• The severity of angina is based on the precipitating activity and its effect on activities
of daily living

- Pathophysiology:
• Angina caused by atherosclerotic disease, associated with a significant obstruction of a
major coronary artery
• The myocardium extracts a large amt of O2 from the coronary circulation to meet its
continuous demands. When there’s an increased in demand, flow through the coronary arteries
needs to be increased
• When there is blockage in a coronary artery, flow cannot be increase and ischemia results

- Clinical manifestations and assessment:

• Pain (mild indigestion) to a choking or heavy sensation in the upper chest
• The pain or discomfort is poorly localized and may radiate to the neck, jaw, shoulders and
inner aspects of upper arm (left arm)
• Feels tightness or a heavy, choking, or strangling sensation
 • Diabetes pt may not have sever pain w/angina b/c diabetic neuropathy can dull the
perception of pain
• The nurse is alert for complaints of unusual fatigue, weakness or numbness in the arms,
wrists and hands; SOB; pallor; diaphoresis; anxiety; dizziness or lightheadedness, N/V that
may accompany the pain (associated S/S)
• The diagnosis of angina begins w/the pt’s history R/T the clinical manifestation of
ischemia. A 12-lead ECG and blood lab biomarker values help in making the diagnosis
• The pt may undergo an exercise or pharmacologic stress test in which the heart is monitored
by ECG
• The pt may referred for a nuclear scan or invasive procedure (cardiac catheterization,
coronary artery angiography)

- Medical management:
• To decrease O2 demand o the
therapy and control of risk
• PCI procedure (percutaneous
placement, atherectomy) and
artery lesions
myocardium and to increase O2 supply, met through pharmacologic
factors
transluminal coronary antipathy [PTCA] with intracoronary stent
CABG. PCI is the preferred method of tx for pt w/simple corona

• Pharmacologic therapy:
Positive inotrope: a med that increases myocardial contractility (force of contraction)
Negative inotrope: A med that decreases myocardial contractility
Positive chronotrope: a med that increase HR
Negative chronotrope: a med that decrease HR

Nitrates:
➡ Mainstay for tx of coronary ischemia
➡ A vasoactive agent (Nitroglycerin) is administered to reduce myocardial O2
consumption, which decrease ischemia and relieve pain
➡ Nitroglycerin dilates the vein (cause venous pooling of blood throughout the body).
As a result, less blood returns to the heart and filling pressure (preload) is
reduced
➡ If the pt is hypovolemic, the decease in filling pressure can cause a significant
decrease in CO and BP, it’s important for the nurse to monitor the pt’s response to
nitrates.
➡ Nitrates relax the systemic arteriolar bed and increase O2 supply
➡ When nitroglycerin is administered sublingually, the pt’s response is assessed
(relief of chest pain and effect on BP and HR). Review box 14-3 for self-
administration of nitroglycerin

Beta-adrenergic blocking agents

➡ beta-blockers such as metoprolol (Lopressor, Toprol) and atenolol (Ternormin) reduce
myocardial O2 consumption by blocking beta-adrenergic sympathetic stimulation to the
heart
➡ The result is a resection in HR, slow condition of impulses through the conduction
system, decreased BP, and reduced myocardial contractility (negative inotrope and
negative chronotrope) to balance the myocardial O2 needs and the amt of O2 available
➡ This helps control chest pain and delays the onset of ischemia during work or
exercise
➡ Reduce the incidence of recurrent angina, infarction, and cardiac mortality
➡ Pt taking these drugs are cautioned not to stop taking them abruptly b/c angina may
worsen and MI may develop

Calcium-channel blocking agents:

➡ Decrease sinoatrial node automaticity and atrioventricular node conduction, resulting
in a slower HR and a decrease in the strength of the heart muscle contraction
(negative inotrope and negative chronotrope effect). These effect decrease the
workload of the heart
➡ Relax the blood vessels, causing a decrease in BP and an increase in coronary artery
perfusion
➡ Increase myocardial O2 supply by dialing the smooth muscle wall of the coronary
arterioles, decrease myocardial O2 demand by reducing systematic arterial pressure
and the workload of the left ventricle
➡ Prescribed to prevent and treat vasospasm
➡ Medications: amlodipine (Norvasc) and diltiazem (Cardizem, Tiazac)
 Antiplatelet and anticoagulant med:
➡ Administered to prevent platelet aggregation and thrombosis, which impedes blood flow
➡ The pt receives anticoagulation therapy should be monitored for S/S of external and
internal bleeding (i.e. low BP, increase HR, decreased hemoglobin and hematocrit)
➡ The pt should placed on bleeding precautions, which include:
Apply pressure to the site of any needle puncture for a longer time than usual
Avoid IM injection
Avoid tissue injury and bruising from trauma or use of constrictive devices
➡ Examples of anti platelet and anticoagulant: aspirin, clopidogrel, heparin,
glycoprotein, and IIb/IIIa inhibitors

Oxygen administration
➡ Initiated at the onset of chest pain to increase the amount of O2 delivered to the
myocardium and to decrease chest pain
➡ Blood oxygen saturation is monitored by pulse oximetry, the normal O2 saturation lv
is greater than 95%

Assessing Angina:
Acronym Factors about pain that need to be assessed Assessment questions

P Position/Location Where is the pain? Can you point to the pain?

Provocation/Palliation What were you doing when the pain began?
What makes it worse?
What makes it better?

Q Quality How would you describe the pain?

Quantity Is it like any pain you had before?
Is it like any pain you had before?
Has the pain been constant?

R Radiation Can you feel the pain anywhere else?

S Severity How would you rate the pain on 0-10 scale?

Symptoms Dis you notice any other symptoms with the pain?

T Timing How long ago did the pain start?

✦ Coronary Artery Disease/Angina Pectoris

- Management of CAD and Angina
- Percutaneous Coronary Interventions (PCIs): immediate intervention
• Balloon angioplasty with intracoronary stent implantation. Occlude coronary artery is
opened and repercussion to the area that had been deprived of O2 is re-established.
The duration of O2 deprivation is directly R/T the # of cells dies. Therefore, the time
from the pt’s arrival in ER department tot he time PCI is performed is critical and
should be less than 60 mins (time is muscle). Referred to as “door-to-balloon” time or
“time-to-device”

- Diagnostic cardiac cauterization and percutaneous coronary intervention:

• A cardiac cauterization is a diagnostic procedure carried out tin the cardiac cauterization
lab where a vascular catheter is inserted in an artery (radial or femoral) and threaded
through your blood vessel to your heart; dye is even on fluoroscopy (x-ray) is then
injected, and the structures of the heart and the potency of the coronary arteries are
visualized
• A stent is then delayed to maintain potency of the artery
• The blood sully to the coronary artery decrease while the ballon is inflated, the pt may
complain of chest pain an dECG may display significant ST segment changes
• Intracoronary stents are usually positioned in the intimate of the vessel to maintain
potency after the ballon is withdrawn

- Coronary artery stent

• After PCI, the area has been treated may potentially close off partially or completely, a
process called restenosis.
• A coronary artery stent is placed to overcome these risk. Restenosis happens in 10%-50% of
pt with PCI after ballon angioplasty w/o stenting, usually within 6 months
 • A stent is a metal mesh that provides structural support to a vessel at risk of acute
closure. Positioned over the angioplasty balloon
• The stent is left permanently in place within the artery, eventually endothelium covers the
stent, and it is incorporated into the vessel wall
• The risk of thrombus formation in the stent, the pt receives antiplatelet meds (aspirin and
clopidogrel), these meds are continued for at least 3-6 months to decrease the risk of
thrombus formation
• Complication occur during PCI procedure: dissection, perforation, abrupt closure, vasospasm
of the coronary artery, acute MI, acute arrhythmias, cardiac arrest. These may require ER
surgical tx
• Complications after the procedure may include abrupt closure of the coronary artery and
vascular complications (i.e. bleeding at the insertion site, retroperitoneal bleeding,
hematoma, pseudoaneurysm, arteriovenous fistula, arterial thrombosis, distal embolization,
acute kidney failure
• Risk factor: elder, female gender, larger vascular sheath size, low BMI, renal
insufficiency, degree of anticoagulation during the procedure

- Post-operative nursing management

• When PCI is performed emergently to relieve acute coronary syndrome (ACS), the pt will go
to critical care unit to be monitored closely for a slightly longer a period of time
• During PCI, pt receive IV heparin and are monitored for sign of bleeding and may receive a
GPIIb/IIIa agent for several hrs following PCI to prevent platelet aggregation and thrombus
formation in the coronary artery and stent

- Coronary artery bypass graft (CABG)

• A surgery used to improve blood flow to the heart in an effort to treat coronary artery
disease 
• A blood vessel is removed or redirects from one area of the body and placed around the area
(s) of narrowing to "bypass" the blockages and restore blood flow to the heart muscle 
• The traditional CABG procedure is performed with the pt under general anesthesia. The
surgeon makes a median sternotomy incision and connects the pt to the cardiopulmonary
bypass machine. A blood vessel form another part of the pt’s body (i.e. saphenous been,
left internal mammary artery) is grafted distal to the coronary artery lesion, bypassing
the obstruction
• CPB is then discontinued, chest tubes & epicardial pacing wires are placed, & the incision
is closed. Pt then is admitted to a critical care unit & typically stays for about 24 hrs
before being transferred to the step-down unit.
• Many cardiac surgical procedures are possible b/c of CPB. The procedure mechanically
circulates & oxygenates blood for the body while bypassing the heart & lungs. CPB maintains
perfusion to body organs & tissues & allows the surgeon to complete the anastomoses in a
motionless, bloodless surgical field.
• CPB is accomplished by placing a cannula in the right atrium, vena cava, or femoral vein to
withdraw blood from the body. The cannula is connected to tubing filled w/ an isotonic
crystalloid solution (usually 5% dextrose in lactated Ringer's soln). Venous blood removed
from the body by the cannula is filtered, oxygenated, cooled, or warmed by the machine, &
then returned to the body. 
• The cannula used to return the oxygenated blood is usually inserted in the ascending aorta,
or it may be inserted in the femoral artery. The heart is stopped by the injection of
cardioplegia soln, which is high in potassium, into the coronary arteries. 
• The pt receives heparin to prevent clotting & thrombus formation in the bypass circuit when
blood comes in contact w/ the foreign surfaces of the tubing. 
• At the end of the procedure, when the pt is disconnected from the bypass machine, protamine
sulfate is administered to reverse the effects of heparin.
• During the procedure, hypothermia is maintained, usually 28°C to 32°C (82.4°F to 89.6°F). The
blood is cooled during CPB & returned to the body. The cooled blood slows the body's basal
metabolic rate, thereby decreasing the demand for oxygen. Cooled blood usually has a higher
viscosity, but the crystalloid solution used to prime the bypass tubing dilutes the blood. 
• When the surgical procedure is completed, the blood is rewarmed as it passes through the
CPB circuit. Urine output, ABGs, electrolytes, & coagulation studies are monitored to
assess the pt's status during CPB.
• Complications:CABG may result in complications such as MI, arrhythmias, hemorrhage, & renal
dysfunction. 
• Although most pts improve symptomatically following surgery, CABG is not a cure for CAD, &
angina, exercise intolerance, or other symptoms experienced before CABG may recur. 
• Meds required before surgery may need to be continued. 
 • Lifestyle modifications recommended before surgery remain important to treat underlying CAD
& for the continued viability of the newly implanted grafts.

✦ Nursing process: The postoperative cardiac surgery pt (review more in pg. 440-442)
- Nursing intervention:
• Restoring CO
• Maintain adequate tissue perfusion
• Maintain normal body temperature
• Monitor and maintain potential complications (infection, fluid volume and electrolyte
imbalance, impaired gas exchange, impaired cerebral circulation)
• Minimize sensory-perception imbalance
• Relieve pain

✦ Myocardiac infarction (MI), review focused assessment box 14-5 on p. 445

- Definition: coronary occlusion, heart attack, and MI

- Pathophysiology:
•  In an MI, an area of the myocardium is permanently destroyed. MI is usually caused by
reduced blood flow in a coronary artery due to rupture of an atherosclerotic plaque &
subsequent occlusion of the artery by a thrombus. 
• In unstable angina, the plaque ruptures, but the artery is not completely occluded. B/c
unstable angina & acute MI are considered to be the same process but occurring at different
points along a continuum, the term acute coronary syndrome may be used in lieu of these
diagnoses. 
• Other causes of MI include vasospasm (sudden narrowing) of a coronary artery, decreased
oxygen supply (e.g., from acute blood loss, anemia, or low BP), & increased demand for
oxygen (e.g., from a rapid HR, thyrotoxicosis, or ingestion of cocaine). In each case, a
profound imbalance exists b/w myocardial oxygen supply & demand.
• The area of infarction develops over min to hrs. As the cells are deprived of oxygen,
ischemia develops, cellular injury occurs, & the lack of oxygen results in infarction, or
the death of cells.
• The expression "time is muscle" reflects the urgency of appropriate treatment to improve pt
outcomes. Each yr in the US, nearly 900,000 ppl have acute MIs; one-fourth of these ppl die
of MI. Half of those who die never reach a hospital.
• Various descriptions are used to further identify an MI: the type of MI (ST-segment
elevation, non-ST-segment elevation), location of the injury to the ventricular wall
(anterior, inferior, posterior, or lateral), point in time within the process of infarction
(acute, evolving, or old), & extent of the damage to the myocardium caused by the MI
(partial or full thickness). 
• Partial infarcts are associated w/ severely narrow coronary arteries & present as non-ST-
segment elevation, while full thickness infarcts commonly occur w/ obstruction of a single
coronary artery & present as ST elevation on ECG readings
• The ECG usually identifies the type & location, & other ECG indicators such as a Q wave &
pt hx identify the timing.
• Regardless of the location of the infarction of cardiac muscle, the goal of medical therapy
is to prevent or minimize myocardial tissue death & to prevent complications.

- Risk factors: the same as those described for atherosclerosis and angina

- Manifestations and assessment:

• Chest pain that occurs suddenly & continues despite rest & med is the presenting symptom in
most pts w/ an MI. 
• Some of these pts have prodromal (early nonspecific) symptoms or a previous dx of CAD, but
about half report no previous symptoms.
• In many cases, the s/s of MI cannot be distinguished from those of unstable angina. 
• The dx of MI is generally based on the presenting symptoms, physical findings, ECG, & lab
test results (e.g., serial cardiac biomarker values). 
• The prognosis depends on severity of coronary artery obstruction & extent of myocardial
damage.

- Diagnosis:
• Patient history:
Pt hx has 2 parts: Description of presenting symptom(s) (i.e. pain) & the hx of
previous illnesses & fam hx of heart disease.
Pt's risk factors for heart disease should also be evaluated
• ECG:
ECG provides info that assists in diagnosing acute MI. It should be obtained within 10
min from the time a pt reports pain or arrives in the emergency dept. 
By monitoring serial ECG changes over time, the location, evolution, & resolution of an
MI can be identified & monitored. The ECG changes that occur w/ an MI are seen in the
leads that view the involved surface of the heart. 
Extent of ischemia & resultant injury through the various layers of the heart determine
the type of ECG changes seen. The classic ECG changes are T-wave inversion, ST-segment
elevation, & development of an abnormal Q wave (Fig. 14-10). 
The 1st ECG signs of an acute MI occur as a result of myocardial ischemia & injury. As
the area becomes ischemic, myocardial repolarization is delayed, causing the T wave
(represents ventricular depolarization) to invert. The ischemic region may remain
depolarized while adjacent areas of the myocardium return to the resting state. 
As ischemia progresses to injury, the T wave becomes enlarged & symmetric. Myocardial
injury also causes ST-segment changes. The ST segment may rise at least 1 mm above the
isoelectric line (area b/w T wave & the next P wave is used as the reference for the
isoelectric line), or there may be non-ST-segment elevation. 
Remember that there may be a combo of ischemia, injury, & infarction occurring
simultaneously, thus resulting in mixed ECG patterns.
The beginning of the ST segment is usually identified by a change in the thickness or
angle of the terminal portion of the QRS complex & is called the J point (Fig. 14-11).
The J point is the end of ventricular depolarization (QRS) & the beginning of the
ventricular repolarization (ST segment) & is identified by a change from an essentially
vertical angle (QRS) to a more horizontal angle (ST segment). 
This J point is normally on the baseline, & elevation in the ST segment in 2 contiguous
leads is a key diagnostic indicator for MI. Nurse assesses for ST elevation, as it
relates to the isoelectric line, at a point 0.08 sec past the J point.
The appearance of abnormal Q waves is another indication of MI. A Q wave is a negative
deflection that signals the beginning of ventricular depolarization; however, abnormal
Q waves represent myocardial necrosis & can develop within 1 to 3 days of an MI.
A pathological Q wave is identified by an abnormal depth & duration of the Q wave or
the appearance of "new" Q waves not previously seen in ECG tracings.The pathological Q
wave therefore reflects the conduction from other parts of the heart, b/c of necrotic
tissue. 
An abnormal Q wave is 0.04 seconds or longer, 25% of the R-wave depth (provided the R
wave exceeds a depth of 5 mm), or did not exist before the event.
An acute MI may also cause a significant decrease in the height of the R wave. During
an acute MI, injury & ischemic changes are usually present. An abnormal Q wave may be
present without ST-segment & T-wave changes, which indicates an old, not acute, MI. 
For some pts, there are no persistent ECG changes, & the MI is diagnosed by blood lvls
of cardiac biomarkers.
Using the above info, pts are diagnosed w/ 1 of the following forms of ACS
1) Unstable angina: pt has clinical manifestations of coronary ischemia, but ECG or
cardiac biomarkers show no evidence of acute MI.
2) ST-segment elevation MI (STEMI): pt has ECG evidence of acute MI w/ characteristic
changes in 2 contiguous leads on a 12-lead ECG. In this type of MI, significant
damage to the myocardium occurs
3) Non-ST-segment elevation MI (non-STEMI): pt has elevated cardiac biomarkers but no
definite ECG evidence of acute MI.
During recovery from an MI, the ST segment often is the first ECG indicator to return
to norm (1 to 6 wks). The T wave becomes large & symmetric for 24 hrs, & it then
inverts within 1 to 3 days for 1 to 2 wks. Q-wave alterations are usually permanent. An
old ST-segment elevation MI is usually indicated by an abnormal Q wave or decreased
height of the R wave w/o ST-segment & T-wave changes.

• Echocardiogram:
Echocardiogram is used to evaluate ventricular function. 
It may be used to assist in diagnosing an MI, esp when the ECG is nondiagnostic.
The echocardiogram can detect hypokinetic & akinetic wall motion, can determine the
ejection fraction, & can also assess valvular function.

• Lab test:
Lab tests called cardiac biomarkers are used to dx an MI.
Newer lab tests w/ faster results, & thus producing earlier dx, include troponin
analysis. These tests are based on the release of cellular contents into the
circulation when myocardial cells die.
 Creatine kinase and its isoenzymes:
➡ Creatinine kinase-myocardial band (CK-MB) is the cardiac-specific isoenzyme; CK-MB is
found mainly in cardiac cells & therefore increases only when there has been damage
to these cells. 
➡ Elevated CK-MB assessed by mass assay is an indicator of acute MI; its lvl begins to
increase within a few hrs & peaks within 24 hrs of an MI. A normal CK-MB is 0 to 3
ng/mL or 1 to 3 μg/L.
➡ If the pt has cardiac complaints & negative CK-MB for more than 48 hrs, then
etiologies for symptoms outside of an MI will be assessed

Myoglobin:
➡ Myoglobin is a heme protein that helps transport oxygen. Like CK-MB enzyme, myoglobin
is found in cardiac & skeletal muscle. A normal lvl is 5 to 70 ng/mL or 5 to 70 μg/
L. 
➡ The myoglobin lvl starts to increase within 1 to 3 hrs & peaks within 12 hrs after
the onset of symptoms. An increase in myoglobin is not very specific in indicating an
acute cardiac event; however, negative results are an excellent parameter for ruling
out an acute MI.
Troponin:
➡ Troponin, a protein found in the myocardium, regulates the myocardial contractile
process. There are three isomers of troponin: C, I, & T. 
➡ Troponins I & T are specific for cardiac muscle, & these tests are currently
recognized as reliable & critical markers of myocardial injury. A normal troponin I
lvl is less than 0.5 ng/dl. 
➡ An increase in the lvl of troponin in the serum can be detected within a few hrs
during acute MI. It remains elevated for a long period, often as long as 3 wks, & it
therefore can be used to detect recent myocardial damage
➡ Troponin I lvls of greater than 1.5 ng/mL or greater than 1.5 μg/L are critical

- Management:
• Goal of medical management is to minimize myocardial damage, preserve myocardial function,
& prevent complications. 
• They may be achieved by reperfusing the area w/ emergency use of thrombolytic meds or by
PCI. 
• Minimizing myocardial damage is also accomplished by reducing myocardial oxygen demand &
increasing oxygen supply w/ meds, oxygen admin, & bed rest
• The resolution of pain & ECG changes indicate that demand & supply are in equilibrium; they
may also indicate reperfusion.
 
• Pharmacologic therapy:
Pt w/ suspected MI is given aspirin, nitroglycerin, morphine, a beta blocker, & other
meds as indicated while dx is being confirmed. 
Pts should receive a beta blocker initially, throughout hospitalization, & upon
discharge. 
Also on discharge, there needs to be documentation that the pt was discharged on a
statin, an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor
blocking agent (ARB), & aspirin. These are "quality indicators" for ACS treatment, &
are now publicly reported measures. 
Remember SAAB: statin, ace or arb, aspirin, beta blocker. If any of these are not
prescribed, clear documentation as to why not must be provided.

• Thrombolytics:
Purpose of thrombolytics is to dissolve & lyse the thrombus in a coronary artery
(thrombolysis), allowing blood to flow through the coronary artery again (reperfusion),
minimizing the size of the infarction, & preserving ventricular function. 
Hospitals monitor their ability to administer these meds within 30 mins from the time
the pt arrives in the emergency dept (called door-to-needle time).
Thrombolytic agents used most often are alteplase (t-PA, Activase) & reteplase (r-PA,
TNKase)

• Analgesic:
Analgesic of choice for acute MI is morphine sulfate administered in IV boluses to
reduce pain & anxiety. It reduces preload & afterload, which decreases the workload of
the heart. 
 Morphine also relaxes bronchioles to enhance oxygenation. The CV response to morphine
is monitored carefully, particularly the BP, which can decrease, & resp rate, which can
be depressed. 
B/c morphine decreases sensation of pain, ST-segment monitoring may be a better
indicator of subsequent ischemia than assessment of pain.

• Angiotensin-Converting Enzyme inhibitors:

ACE inhibitors prevent the conversion of angiotensin I to angiotensin II. In the
absence of angiotensin II, BP decreases & the kidneys excrete sodium & fluid
(diuresis), decreasing the oxygen demand of the heart. 
Use of ACE inhibitors in pts after MI decreases mortality rates & prevents remodeling
of myocardial cells, which is associated w/ the onset of heart failure. 
Important to ensure that the pt is not hypotensive, hyponatremic, hypovolemic, or
hyperkalemic before administering ACE inhibitors. 
BP, urine output, & serum sodium, potassium, & creatinine lvls need to be monitored
closely. An ARB can be used in lieu of an ACE inhibitor

✦ The nurse caring for a patient with an MI knows that at the top priority in the care of this
patient is which of the following?
A. balancing intake and output
B. Decreasing energy expenditure of the myocardium
C. Balancing myocardial oxygen supply with demand???
D. Decreasing nutritional need of myocardial muscle
Heart failure
✦ Heart failure/Congestive heart failure: the inability of the heart to pump sufficient blood to meet
the needs of the tissue of O2 and nutrients
- Characterized by S/S of fluid overload or of inadequate tissues perfusion
- Fluid overload and decreased tissue perfusion result when the heart cannot generate a cardiac
output sufficient to meet the body’s demand
- Heart failure indicated myocardial disease in which there’s a problem with contraction of the
heart (systolic dysfunction) of filling of the heart (diastolic dysfunction) that may or may
not cause pulmonary or systemic congestion
- HF is progressive, lifelong diagnosis that is managed with lifestyle changes and meds to
prevent acute congestive episodes

✦ Chronic heart failure

- The nature of chronic heart failure can be either systolic or diastolic with systolic failure
the most common at 60%
- In the U.S., the lifetime risk of developing HF is 20% for those age 40 years and older
- HF is the most common reason for hospitalization of ppl older than 65 years of age and the
second most common reason for visits to a health care provider

✦ Two types of HF:

- Identified by assessment of left ventricular functioning, usually by echocardiogram
- The more common type is an alteration in ventricular contraction (systolic heart failure),
characterized by a weakened heart muscle
- The less common alteration is diastolic heart failure, which is characterized by a stiff and
noncompliant heart muscle, making it difficult for the ventricle to fill
- An assessment of ejection fraction (EF) is performed to assist in determining the types of HF
• EF, an indication of volume of blood ejected with each contraction, is calculated by
subtracting the amt of blood at the end of systole from the amt at the end of diastole and
calculating the % of blood that is ejected.
• A normal EF is 50-70% of the ventricular volume, the ventricle does not empty completely
btwn contractions
• The EF is normal in diastolic HF but severely reduced in systolic HF
• Although a low EF is hallmark/fundamental pathophysiologic abnormality of all HF, the
severity of HF classified according to the pt’s symptoms
• The EF is normal in diastolic HF but severely reduced in systolic HF
• Pathophysiology alert: In diastolic heart failure there is a normal or equate to normal CO.
A normal EF is not a reliable gauge of normal CO. The nurse is aware that a low CO is the
fundamental pathophysiologic abnormally of all HF

✦ Pathophysiology
- HF results from a variety of cardiovascular conditions (including chronic hypertension, CAD,
valvular disease, congenital heart defects, and arrhythmias) and from conditions (i.e. diabetes
mellitus, fever, infection, thyrotoxicosis, iron overload, hypoxia, anemia, and pulmonary
embolus)
- These conditions can result in decreased contraction (systole), decreased filling (diastole) or
both. Significant myocardial dysfunction occurs before the pt experiences S/S of HF (i.e. SOB,
edema, fatigue)
- As HF develops, the body activates neurohormonal compensatory mechanism, which represent the
body’s attempt to cope with HF & are responsible for the S/S that eventually develop
- Systolic HF results in a decrease in the volume of blood being ejected from the ventricle. The
decreased ventricular stretch is sensed by baroreceptors (sensors in blood vessels that respond
to perfusion pressure of blood flow) in the aortic and carotid bodies
- The sympathetic nervous system is stimulated to release epinephrine and norepinephrine . The
purpose of this initial response is to increase HR & contractility & support the failing
myocardium
- Sympathetic stimulation causes vasoconstriction of the skin, GI tract, & kidneys
- A decrease in renal perfusion due to low CO & vasoconstriction then causes the release of renin
by the kidneys
- Renin promotes the formation of angiotensin I, a benign, inactive substance
- Angiotensin-converting enzyme converts angiotensin I to angiotensin II, which then increase the
BP & afterload
- Angiotensin II stimulates the release of aldosterone form the adrenal cortex, resulting in
retention of Na+ & fluid, excretion of K+ by the renal tubules, and stimulation of the thirst
center. Which leads to fluid volume overload commonly seen in HF
 - Angiotensin, aldosterone, and other neurohormones lead to an increase in preload and afterload,
which increases stress on the ventricular wall, causing an increase in the workload of the
heart
- As the heart’s workload increase, contractility of the myocardial muscle fibers decreases
(result in an increase in end-diastolic blood volume (preload) in the ventricles, stretching
the myocardial muscle fibers & increase the size of the ventricle (ventricular dilation))
- The increased size of the ventricle increases the stress on the ventricular wall, adding to the
workload of the heart
- The heart compensates for the increase workload is to increase the thickness of the heart
muscles (ventricular hypertrophy)
- Hypertrophy results in an abnormal proliferation of myocardial cells, known as ventricular
remodeling
- Diastolic HF develops b/c of continued increased the workload on the heart, which responds by
increasing the number & size of myocardial cells
- These responses cause resistance to ventricular filling, which increases ventricular filling
pressures despite a normal or reduced blood volume
- Less blood in the ventricles caused decreased CO

✦ Risk factors:
- Risk factors that are asymptomatic for HF are included in stage A HF
• Hypertension (more profound in women, encouraged to maintain their BP below 140/90 mmHg
consistently)
• Diabetes mellitus or metabolic syndrome
Metabolic syndrome is confirmed in pt who have any 3 of the following:
➡ abdominal obesity
➡ elevated triglyceride level (over 150 mg/dL)
➡ decreased HDL (<40 mg/dL for men, <50 mg/dL for women)
➡ HTN and elevated fasting glucose
• Those with atherosclerotic disease (CAD, stroke, or peripheral vascular disease) are likely
to develop HF w/o adequate control of CV risk. It’s important to note that the primary
cause of HF in men is CAD

Comparison of systolic and diastolic heart failure

Systolic Failure Diastolic Failure

Pathophysiology • Impaired ventricular pumping of blood • Impaired ventricular relaxation filling

during systole
• Characterized by reduced stroke volume,
incomplete ventricular emptying, cardiac
dilation, and elevated left ventricular
diastolic pressure
• Reduced CO evokes compensatory
neurohormonal responses that increase HR,
Na+ and H2O retention, & vasoconstriction
during diastole
• Characterized by a stiffened left
ventricle that cannot relax and fill
sufficiently at normal diastolic
pressure
• The result is either decreased left
ventricular end-diastolic volume
(leading to decreased CO) or a
compensatory rise in left ventricular
filling pressure, which can lead to
pulmonary venous HTN

Causes/etiology • Usually caused by ischemic or idiopathic • Usually caused by hypertensive,

dilated cardiomyopathy, when the left hypertrophic, or restrictive
ventricle cannot adequately contract or cardiomyopathy
squeeze out its contents, so that preload
increases and stroke volume decreases

✦ Clinical manifestation and assessment

- Resting dyspnea, cyanosis, cachexia (physical wasting), resulting from long-standing heart
disease
- A baseline height and weight should be documented on admission and with rechecked each morning
- Obtaining daily weights and tracking trends in weight, along with an accurate I&O log, provide
an easy and accurate way to monitor fluid balance
• Nursing alert: Daily weights should be at the same time, on the same scale, and with the
patient wearing the same clothes for accuracy. The nurse is aware that when calculating new
gain or loss that 500 mL approximates 1 lb or 1000 mL approximates 1 kg (2.2 lb)
- Fluid balance is an important surveillance strategy in controlling Hf symptoms
 - BP measurement in both sitting and standing positions in order to detect orthostatic
hypotension
- Tachycardia (HR over 120 ppm) may signal worsening HF. When HR is rapid, SV decrease b/c the
ventricle has less time to fill. In turn, produces increased pressure in the atria and in the
pulmonary vascular bed
- A weak, thready pulse and pulses alternans (pulse is regular but force of amplitude varies with
alternating beats form large to small) are signs of decreased left ventricular function
- Left ventricular hypertrophy may displace the apical pulse left and downward form its normal
location at the 5th intercostal space, medial to the midclavicular line
- Right-sided HF may present with elevation in jugular venous pressure greater than 4 cm above
the sternal angle
- An S3 heart beat is a sign that the heart is beginning to fail and increased blood volume is
filling the ventricle with each beat (mitral and tricuspid regurgitation murmur)
- An S4 sound is when the pt has increased resistance to ventricular filling b/c of increased
stiffness of the ventricular myocardium

- The nurse assesses the lungs

• Crackles/rales are discrete, discontinuous crackling sounds heard at the end of
inspiration, produced by the sudden delayed reopening of edematous small airways and
alveoli and are not cleared with coughing
• It’s recommended to being auscultated at the base of the lungs to detect crackles in HF pt
and notes the extent. Crackles start at the lung bases and are heard progressively higher
in the lungs as HF worsens
• Wheezing may also heard in some pt
• The rate and depth of respirations are also documented
• Dullness to percussion may indicate pleural effusions due to HF
- The nurse assesses dependent parts of the pt’s body for perfusion and edema
• With significant decrease in SV, there’s a decrease in perfusion to the periphery, which
causes the skin to feel cool and appear pale/cyanotic
• If the pt sit upright, the feet and lower legs are examined for edema
• If the pt is supine in bed, the sacrum and back are also assessed for edema
• Fingers and hands become edematous. The nurses notes the location and extent of the edema
and assessed for evidence of pitting edema
- Hepatomegaly, hepatojugular reflux, and ascites can occur with venous congestion due to right-
sided HF (there’s accumulation of fluid in the systemic venous circulation)
• To assess hepatojugular reflux, the pt is asked to breath normally while manual pressure is
applied over the right upper quadrant of the abdomen for at least 5 secs
• If the top of the jugular venous column in the neck res and persists as long as the
abdominal pressure is continued, it’s considered positive hepatojugular reflux, indicating
the right ventricle cannot accommodate the additional volume of displaced blood
• A positive hepatojugular flux is associated with right HF and constrictive pericarditis
- Sensorium and LOC must be evaluated. Pt may complain of dizziness and lightheadedness

Symptom comparison of left- versus right-sided heart failure

Left-sided HF Right-sided HF

Pathophysiology • Pulmonary congestion from • Right ventricle pump failure leading to

impaired left ventricle (LV)
function
• LV cannot pump blood out of
ventricle effectively into the
aorta and the systemic
circulation
• Pulmonary venous blood volume and
pressure increase, forcing fluid
from the pulmonary capillaries
into the pulmonary interstitial
edema and impaired gas exchange
congestion in the peripheral tissues and the
viscera
• Right side of the heart cannot eject blood and
cannot accommodate all the blood that normally
returns to it form the venous circulation
• Increased venous pressure leads to jugular vein
distension (JVD) and increased hydrostatic
pressure throughout the venous system. Normal
central venous pressure (CVP) is 2-8 mmHg. A CVP
greater than 8 mmHg associated with hypervolemia
(excessive fluid circulating in the body) or
right-sided HF
Left-sided versus Right-sided HF:
- Left-sided HF
• Dyspnea, orthopnea, PND
• Cough
• Pulmonary crackles (raleS)
• Decrease O2 saturation levels
• S3 ventricular gallop
• Oliguria, if kidney perfusion is diminished
• Decreased perfusion to other systemic organs (advanced failure):
Sluggish GI motility
Dizziness, lightheadedness, confusion, restlessness
Anxiety
Skin cool and clammy
Decrease in EF
Tachycardia or weak/thready pulse
Fatigue or activity intolerance

- Right-sided HF
• Lower extremity dependent edema (dependent edema is swelling that follows the position of the
body):
Legs and feet
May progress to thighs, eternal genitalia, lower trunk, abdomen, and sacral edema (in a bed-
bound pt)
Pitting edema (indentations in the skin remain even after slight compression with the
fingertips)
• Hepatomegaly (enlargement of the liver)
• Ascites (accumulation of fluid in the peritoneal cavity)
• Anorexia and nausea
• Weight gain due to retention of fluid
• Weakness/fatigue from reduced CO & impaired cognition
• Decreased perfusion to other systemic organs (advanced failure)

✦ Diagnostic evaluation:
- A chest X-ray: determine the presence and extend of cardiac enlargement or pulmonary congestion
and can help identify pulmonary disease. (Cardiomegaly: systolic dysfunction, normal heart
size: diastolic dysfunction)
- A 12-lead electrocardiogram (ECG): determine the presence of cardiac arrhythmias, LVH, and
previous or current MI. (If the pt has left ventricular dysfunction, ECG indicates a left
ventricular electrical abnormality specific to ventricular dilation or hypertrophy)
- A two-dimensional (2D) echocardiogram with Doppler”: a noninvasive test to look for structural
cardiac abnormalities and to measure EF (An EF of less than 40% indicates systolic dysfunction;
an EF of greater than 40% with S/S of HF and impaired ventricular relaxation indicates
diastolic dysfunction
- Cardiac magnetic resonance testing: gold standard for assessing cardiac fxn, more expensive
- Laboratory tests: help diagnose HF (CBC; electrolyte level- Ca+2, Mg+2; BUN; creatinine; serum
glucose; serum albumin; liver fxn tests; thyroid-stimulating hormone; urinalysis; BNP levels)
- A right-sided heart catheterization: determine the heart’s preload pressure and pulmonary
pressures to determine the degree of HF and the need for further intervention

✦ Management:
- Tx begin with prevention. identifying pt at risk is the first step in the care and Tx of HF
- The overall goals of management of HF are to relieve pt symptoms, improve functional status, &
quality of life and extend survival
- Tx is based on the type, severity, and cause of HF:
• Eliminate or reduce any ectopic contributory factors especially those that may be
reversible (i.e. atrial fibrillation, excessive alcohol ingestion, uncontrolled HTN)
• Reduce the workload on the heart by reducing afterload and preload
• Optimize all therapeutic regimens
• Prevent exacerbation of HF

- Lifestyle changes:
• Provide general education and counseling to the pt and family
• Restriction of dietary sodium, and smoking; weight reduction when indicated; and regular
exercise
 • Know how to recognize S/S that need to be reported to the health care professional (i.e.
weight gain, increasing SOB, fatigue and edema
- Pharmacologic therapy:
• Meds prescribed routinely for systolic HF (i.e. ACE inhibitors, beta blockers, diuretics,
and digoxin)
• Meds for diastolic failure depend on the underlying conditions (i.e. HTN or vascular
dysfunction)

✦ Nursing management:
- Assessing the patient
• Observe for effective of therapy and for he pt’s ability to understand and implement self-
management strategies
• S/S of pulmonary & systemic fluid overload are recorded and reported immediately
• Explores the pt’s emotional response to the diagnosis of HF, a chronic and often
progressive condition
• The health history focuses on S/S of HF (i.e. SOB, dyspnea on exertion, SOB occurs with
exertion, cough)
• Sleep disturbances (sleep interrupted by SOB) is called paroxysmal nocturnal dyspnea may be
reported
• Ask about the number of pillows needed for sleep (an indication of orthopnea— SOB while
lying flat), edema, abdominal symptoms, altered mental status, actives of daily living,
daily weight, and the activities that cause fatigue
• Help pt identify the impact the illness has had on their quality of life and successful
coping skills they have used
- Monitoring intake and output
• Monitor I&O
• Must monitor for oliguria (diminished urine output, less than 400 mL/24 hr) or anuria
(urine output less than 100 mL/24 hr)
• A significant change in weight (i.e. 2 to 3 lb increase in a day or 5 lb increase in a
week), the pt is instructed to notify PCP or to adjust the med (i.e. increase the diuretic
dose) per the provider’s directions

✦ The nurse’s assessment of an older adult patient reveals multiple risk factors for HF. Which of the
following risk factors should the nurse address in patient teaching?
A. The patient’s age
B. The patient’s racial background
C. The patients sex
D. The patient’s diabetes management

Heart disease complications

✦ Pulmonary edema:
- Definition: the abnormal accumulation of fluid in the lungs, this fluid may accumulate in the
interstitial spaces and in the alveoli. Can be categorized into cardiogenic and non-cardiogenic

- Pathophysiology:
• Cardiogenic pulmonary edema is an acute event that results from HF, occur acutely (i.e. MI)
or it can occur as an exacerbation of chronic HF
• With increased resistance to left ventricular filing, blood backs up into the pulmonary
circulation. The pt quickly develops pulmonary edema (flash pulmonary edema), from the
blood volume overload in the lungs
• Pulmonary edema can be caused by noncardiac disorders (i.e. kidney failure, liver failure,
and oncologic conditions that cause the body to retain fluid)
• Left ventricle cannot handle the volume overload, and blood volume and pressure build up in
the left atrium
• Impaired lymphatic drainage contributes to the accumulation of fluid in the lung tissues.
The fluid within the alveoli mixes w/air, creating “bubbles” that are expelled from the
mouth and nose, produce symptom of pulmonary edema, frothy sputum, alveoli are flooded with
fluid from capillaries, producing thin secretions containing air bubbles that are colored
with hemoglobin
• B/c fluid within alveoli, air cannot enter, gas exchange is impaired. Resulting in
hypoxemia
• The onset may be preceded by premonitory symptoms of pulmonary congestion, it may develop
quickly in the pt with a ventricle that has little reserve to meet increased oxygen levels

- Clinical manifestations and assessment:

• Restless, anxious
 • Sudden onset of breathlessness, a sense of suffocation
• Cough that produces a large amount of frothy sputum (can be blood tinged)
• Cold and moist skin, cyanotic (bluish) nail beds
• Weak and rapid pulse
• Pulmonary crackles (rales), expiratory wheezing, and distended neck veins
• O2 saturation decreased

- Medical and nursing management:

• Clinical management plan for treating acute decompensated HF (O2, diuretics, pharmacologic
preload and afterload reduction, hemodynamic monitoring
• Early rescue with noninvasive mask ventilation and bronchodilator therapy with select beta2
agonist medication like albuterol

✦ Cardiogenic shock: (pt in ICU)

- Definition: occurs when decreased CO leads to inadequate tissue perfusion and initiation of the
shock syndrome.
• Occur following MI, when a large area of myocardium becomes ischemic, necrotic, and
hypokinetic (slow or diminished muscle motion)
• Can occur as a result of end-stage HF, cardiac tamponade, pulmonary embolism (PE),
cardiomyopathy, and arrhythmias
• Cardiogenic shock is a life-threatening condition with a high mortality rate

- Pathophysiology:
• S/S reflect the circular nature of the pathophysiology of HF
• The heart muscle loses its contractile power, resulting in a marked reduction in SV and CO
• The decreased CO reduce arterial blood pressure and tissue perfusion in the vital organs
(heart, brain, lung, kidneys)
• Flow to the coronary arteries is reduced, resulting in decreased O2 supply to the
myocardium, which increase ischemia and further reduces the heart’s ability to pump
• Inadequate emptying of the ventricle also lead to increased pulmonary pressures, pulmonary
congestion, and pulmonary edema, exacerbating the hypoxia, causing ischemia of vital
organs, and setting a vicious cycle in motion

- Clinical manifestation and assessment:

• Tissue hypoperfusion and results from HF and the overall shock state
• Cerebral hypoxia (restlessness, confusion, agitation)
• Low BP, rapid and weak pulse
• Cold and clammy skin
• Tachypnea with respiratory crackles and decreased urinary output
• ABG show respiratory alkalosis R/T tachypnea
• Arrhythmias are common and result from myocardial ischemia
• A pulmonary artery catheter inserted to measure CO and hemodynamic parameters that are used
to assess the severity of the problem and to guide pt management
• The pulmonary artery wedge pressure is elevated and CO is decreased as the left ventricle
loses its ability to pump
• The systemic vascular resistance is elevated b/c of sympathetic nervous system stimulation
that occurs as a compensatory response to the decrease in blood pressure
• The decreased blood flow to the kidneys causes a hormonal responses that cause fluid
retention and vasoconstriction
• Increase in HR, circulating volume, vasoconstriction occur to maintain circulation to the
brain, heart, kidneys, and lungs but at a cost: an increase in the workload of the heart

• Continuous central venous oximetry and measurement of blood lactic acid levels may help
assess the severity of the shock and the effectiveness of the Tx
• Continued cellular hypoperfusion results in organ failure. The pt becomes unresponsive,
severe hypotension ensues, and the pt develops shallow respiration and cold, cyanotic and
mottled skin
• Lab tests result indicate organ dysfunction

- Medical management:
• Correct the underlying problem, reduce any further demand on the heart, improve
oxygenation, and restore tissue perfusion
• If the ventricular failure is the result of an acute MI, emergency percutaneous coronary
intervention may be indicated
• Major arrhythmias are corrected b/c they may caused or contribute to the shock
 • If the pt has hypervolemia, diuresis is indicated. Diuretics, vasodilators, and mechanical
therapies (i.e. continuous renal replacement therapy) have been used to reduce the
circulating blood volume
• If the pt have hypovolemia, the patient is given IV volume expanders (i.e. normal saline
solution, lactated Ringer solution, albumin) to increase the amt of circulating fluid. The
pt is placed on strict bed rest to conserve energy
• If the pt has hypoxemia, as detected by pulse oximetry or ABG analysis, O2 administration
is increased. Intubation and sedation may be necessary to maintain oxygenation

✦ Pericardial effusion/cardiac tamponade:

- Definition: (accumulation of fluid in the pericardial sac) may accompany pericarditis, advanced
HF, metastatic carcinoma, chemotherapy, cardiac surgery, trauma

- Pathophysiology:
• The pericardial sac contains less than 50 mL of fluid, which is needed to decrease friction
for the beating heart. An increase in pericardial fluid raises the pressure within the
pericardial sac and compresses the heart. This has following effects:
• Pericardial fluid accumulate slowly w/o causing noticeable symptom until a large amt
accumulates
• Increased pericardial pressure, venous return to the heart is obstructed and the amt of
blood pumped out with each contraction is reduced, which decrease CO. Resulting in cardiac
tamponade (i.e. compression of the heart)

- Clinical manifesting and assessment:

• A feeling of fullness within the chest or may have substantial or ill-defined pain
• Feeling pressure in the chest may result from stretching of the pericardial sac
• Increased pressure within the pericardium, venous pressure tend to increase as well, as
evidenced by engorged neck veins during inspiration “Kussmaul sign”
• Dyspnea, cough, labile or low BP
• Sytolic BP is lower during inhalation is called pulsus paradoxus (exceeding 10 mmHg is
abnormal). A pericardial friction rubs may be heard
• The cardinal signs of cardiac tamponade are falling systolic BP, narrowing venous pressure
(increased JVD) during inspiration, and distant (muffled) heart sounds. If untreated, shock
and death can result
• A chest x-ray shows a large pericardial effusion. An echocardiogram is performed to confirm
the diagnosis

- Medical and nursing management:

• Pericardiocentesis:
Pericardiocentesis (puncture of the pericardial sac to aspirate pericardial fluid) is
performed to remove fluid from the pericardial fluid
The major goal for this procedure is to prevent cardiac tamponade, which restricts
normal heart filling and contraction
The HOB is elevated to 45-60 degrees, placing the heart in proximity to the chest wall
so the needle can be inserted into the pericardial sac
Peripheral IV line is inserted (slow IV infusion) and started in case it becomes
necessary to administer emergency med or blood products
The pericardial aspiration needle is attached to a 50 ml syringe by a three way
stopcock. Ultrasound imaging to guide the placement of the needle
Complications of pericardiocentesis include:
➡ ventricular coronary artery puncture
➡ arrhythmias, pleural laceration
➡ gastric puncture, myocardial trauma
After the procedure, the pt’s heart rhythm, BP, venous pressure, heart sounds are
monitored to detect possible recurrence of cardiac tamponade
Cardiac tamponade may require surgical Tx by open pericardial drainage called
pericardiotomy
• Pericardiotomy:
Recurrent pericardial effusions, associated with neoplastic disease, may be treated by
a pericardiotomy (pericardial window)
Under general anesthesia, a portion of the pericardium is excised to permit the
pericardial fluid to drain continuously into mediastinum and is reabsorbed via
lymphatics

✦ Cardiac arrest:
- Definition: Cardiac arrest occurs when the heart ceases to produce an effective pulse and
circulate blood

- Pathophysiology:
• Caused by a cardiac electrical event (i.e. ventricular fibrillation, progressive profound
bradycardia, when there is no heart rhythms at a all (asystole))
• May follow respiratory arrest, occur when electrical activity is present but there is
effective cardiac contraction or circulating volume, called pulseless electrical activity
(PEA)
• PEA can caused by hypovolemia (i.e. excessive bleeding), hypoxia, hypothermia,
hyperkalemia, massive PE, MI, and med overdose (i.e. beta blockers, calcium-channel
blocker)

- Clinical manifestation and assessment:

• Consciousness, pulse, and BP are lost immediately. Ineffective respiratory gasping may
occur
• The pupils of the eyes begin dilating within 45 secs. Seizure may or may not occur
• The risk of irreversible brain damage and death increase with every min from the time that
circulation ceases

- Emergency management: Cardiopulmonary resuscitation

• CPR provides blood flow to vital organs until effective circulation can be reestablished
• A-B-C (airway-breathing-circulation) was replace with new standard C-A-B (compression,
airway, breathing)
Cardiac disorders
✦ Valvular disease:
- Definition: Acquired valvular heart disease is a chronic, progressive disorder that develop
slowly. Common causes: degenerative disease, rheumatic heart disease, and infective
endocarditis (inflammation of the inner lining of the heart, the endocardium)
- Progression of valvular heart disease can result in heart failure, arrhythmias, stroke, sudden
death
- Intervention for the management and tx of acquired valvular heart disease are aimed at
preventing the sequelae of atrial fibrillation (AF), thromboembolism, pulmonary artery HTN, and
heart failure
- When heart valves do not close or open properly, blood flow is affected. The turbulent flow of
blood through a heart valve opening result in a murmur
- Characteristic stenosis occurs when opening of the valve is narrowed, & the forward flow of
blood through the valve is reduced. 
- The increase in resistance results in turbulent blood flow. The volume of blood in the chamber
increases and the heart is forced to work harder to eject blood through the narrowed valve,
resulting in increased after load and decrease CO
- Regurgitation, or valvular insufficiency, occurs when valves do not close completely & blood
flows backward through the valve.
- If the aortic valve is affected, blood will flow backward into the left ventricle during
diastole, and if mitral valve is affected, blood will flow back into left atrium during
systole. Preload is increased
- Mitral valve prolapse occurs when mitral valve does not close properly and the valve leaflets
balloon back into the LA during systole
- Valvular disorders may require surgical repair or replacement of the valve to correct the
problem, depending on the severity of symptoms
- Pulmonic and tricuspid valve disorders occur. Tricuspid regurgitation occurs with mitral
stenosis b/c of increased volume and pressure load on the right side of the heart but can
result form infective endocarditis
- Tricuspid valve repair is done only if there is severe regurgitation
- Nursing alert: Stenosis is a pressure problem, regurgitation is a volume problem. Blood volume
and pressures are increase behind the affected valve and reduced in front of the affected valve

✦ Mitral stenosis:
- Definition: the valve opening is narrowed, and blood flow from the LA into the LV is slowed
during diastole. MS is slow and progressive. Symptoms may takes decades to appear. Over time,
heart failure will develop

- Pathophysiology:
• Left atrial pressure increases b/c of the slowed blood flow into the LV through the
narrowed orifice. The left atrium dilates & hypertrophies b/c of the increased blood
volume. Sluggish atrial blood flow can lead to clot formation & thromboembolism. 
• B/c there is no functional valve to protect the pulmonary veins from the backward flow of
blood from the atrium, pulmonary venous pressure rises & circulation becomes congested.
• As a result, the RV must contract against an abnormally high pulmonary pressure, & the RV &
right atrium become enlarged. Eventually, this results in right-sided heart failure

- Risk factors:
• Caused by rheumatic fever (RF) or endocarditis, which gradually caused the mitral valve
leaflets to thicken and result in leaflet fusion
• Radiation therapy to the chest area also result in MS
• It is more common in women than in men. Rarely, it can result from a congenital defect

- Clinical manifestation and assessment:

• Symptoms usually develop after valve opening is reduced by 1/3 to 1/2 its usual size. 
• Dyspnea on exertion (DOE) results from pulmonary congestion. Pts become progressively
fatigued as a result of low CO. Paroxysmal nocturnal dyspnea (PND) & a.fib may occur.
Dyspnea at rest is likely w/ severe MS. 
• Other symptoms: heavy coughing, sometimes w/ hemoptysis from ruptured pulmonary veins,
hoarseness from the dilated atrium impinging on the left recurrent laryngeal nerve,
palpitations, orthopnea, & recurrent resp infections.
• Later, symptoms of right HF, including peripheral edema & ascites, occur.
• A loud S1 due to abrupt closure of the mitral valve & an early diastolic opening snap can
be heard. The snap is the premature opening of the stenotic mitral valve.
 • A low-pitched, rumbling, diastolic murmur (heard on S2) is heard best at the apex. The
murmur is caused by turbulent blood flow through the abnormally tight valve opening. 
• Due to the increased blood volume & pressure, the atrium dilates, hypertrophies, & becomes
electrically unstable, leading to atrial arrhythmias. The pulse can be weak & irregular b/c
of a.fib. 
• Echocardiography is the most sensitive & specific noninvasive method to dx MS. Cardiac cath
is not indicated unless clinical findings & echo results are discordant.

✦ Mitral valve disorders

- Mitral valve prolapse:
• Definition: A portion of one or both mitral valve leaflets bulge back into the LA during
systole, usually with little or no mitral regurgitation

• Pathophysiology:
Myxomatous degeneration (pathologic weakening of connective tissue) can cause one or
both of the valve leaflets to become enlarged and floppy, causing them to billow into
the LA during systole
Overtime, as the leaflets prolapse, they can stretch to a degree where the leaflet
edges do not fully coast, or close, resulting in MR

• Risk factors:
Female gender and family history are associated with MVP, often occurs in ppl with
Marfan syndrome, a connective tissue disorder

• Clinical manifestations and assessment:

MVP is commonly asymptomatic
Fatigue, dyspnea, palpitations, chest pain
A typical chest pain is not R/T activity and may be caused by abnormal stress placed on
the chord tendineae and papillary muscles
SOB is not correlated with activity levels or pulmonary fxn
Cardiac auscultation may reveal a mitral midsystolic click. This is a sing that a valve
leaflet is ballooning into the LA
A late systolic murmur may be heard if progressive valve leaflet stretching and
regurgitation have occurred
Echocardiography is used to diagnose and monitor the progression of MVP

- Mitral regurgitation:
• Definition: (mitral insufficiency)
the backward flow of blood from the LV into the left atrium during systole b/c the
valve fails to close completely. 
Disease processes that alter valve leaflets, mitral annulus, chordae tendineae, & the
papillary muscle may result in MR.

• Pathophysiology:
When mitral valve leaflets thicken, fibrose, & contract, they cannot close completely. 
W/ each heartbeat, blood is forced backward into the left atrium during systole.
Regurgitation of blood into the left atrium causes left atrial pressure to rise. 
B/c this blood is added to the blood flowing in from the lungs, the left atrium must
stretch to accommodate the increased volume, & left atrial hypertrophy & dilatation
occur. 
During diastole, regurgitant blood from the atrium increases volume load in the LV.
Over time, compensatory left ventricular hypertrophy occurs to maintain a norm CO.
Eventually this leads to LV failure.
The backward flow of blood from the LV reduces blood volume flowing into the atrium
from the lungs & pulmonary venous pressure increases.
Pulmonary congestion results, elevating pulmonary artery pressure; this adds further
strain on the RV causing enlargement & right ventricular failure

• Risk factors:
More common in older adult and result over time from normal aging
Having MVP or mitral valve stenosis can lead to development of chronic primary MR, most
ppl with MVP never develop severe regurgitation
Rheumatic heart disease can result in thick, rigid mitral valve that does not open and
close completely, leading to MR

• Clinical manifestation and assessment:

 Chronic MR may be asymptomatic for yrs; then, sx gradually develop.
As CO diminishes, fatigue, tachycardia, & weakness can occur. Orthopnea, DOE, &
Paroxysmal nocturnal dyspnea result from pulmonary congestion.
Palpitations are r/t a hyperdynamic LV and/or a.fib.
Peripheral edema & ascites occur when the RV fails. Acute MR manifests as severe left-
sided HF. Pts may report a sudden inability to breathe accompanied by chest pain
Physical exam may reveal a hyperdynamic PMI, displaced leftward & downward b/c of the
hypertrophied LV. A holosystolic murmur (heard on S1) is heard as a high-pitched,
blowing sound at the apex; radiation to the axilla is possible.
An S3 or S4 gallop may be present b/c of increased, rapid blood flow into the ventricle
during diastole.
Signs of left- & right-sided HF are seen in acute MR: tachycardia, crackles, &
hypotension, as well as peripheral edema, JVD, & ascites
Chest X-ray may reveal LV & left atrial enlargement. A transthoracic echocardiogram
(TTE) is used to monitor severity & progression of MR, as well as the anatomy of the
valve. It also provides info regarding LV size & function, left atrial size, &
pulmonary artery pressures. 
A transesophageal echocardiogram (TEE) provides the best images of the mitral valve, &
may be done if the TTE is inconclusive
Cardiac catheterization may be done preoperatively, & may also be used if there is a
discrepancy b/w clinical & noninvasive findings to determine the severity of MR.

✦ Acute mitral regurgitation:

- Definition: occur abruptly, when papillary muscle rupture occurs as a complication of MI or if
infective endocarditis or trauma less to rupture of the chordae tendineae. This is a cardiac
emergency b/c of the sudden and severe hemodynamic compromise, almost symptomatic

- Pathophysiology:
• An acute MI can damage the ventricular wall and disrupt the attachment of the papillary
muscle or the chordae tendineae, resulting in acute MR
• W/o a normally fxn valve to direct the flow of blood forward, a large amt of blood from LV
flow backward into the LA
• This compromises forward flow of blood and CO is diminished, which can lead to cariogenic
shock
• Compensatory mechanism lead to an increase in systemic vascular resistance (SVR), which can
worsen regurgitation
• At the same time, additional blood flows back into LA causes an increase in left atrial
pressure and forces blood back into the pulmonary circulation

- Clinical manifestation and assessment:

• Signs of left- and right-sided HF are seen in acute MR: severe SOB, pallor, tachycardia,
crackles, and hypotension, peripheral edema, jugular venous distention, and ascites
• Poor tissue perfusion is common as acute pulmonary decompensation
• Rapid assessment with an echocardiogram is necessary to establish a diagnosis. LA and
ventricle are normal in size, and systolic function can be hyper dynamic or normal, a fail
leaflet may be seen

✦ Aortic stenosis
- Definition: AS is narrowing of the valve opening b/w the LV & the aorta, resulting in
obstruction of blood flow across the valve.

- Pathophysiology:
• Progressive narrowing of the valve orifice usually occurs over several yrs to several
decades. 
• The LV overcomes this by contracting more slowly & more strongly than norm, forcibly
squeezing the blood through the smaller orifice. 
• This increases LV pressure, & the ventricular wall hypertrophies & dilates. LV failure
ensues. This leads to elevated left atrial pressure, then pulmonary congestion, &
ultimately right HF.

- Risk factors:
• The buildup of calcium deposit on heart valves is the most common case of AS
• As calcification progresses, valve leaflets become more rigid and outflow from LV becomes
obstructed
• Acquired As is common in those over 70 yrs of age, in males
 • Besides degenerate of the valve, rheumatic heart disease can lead to AS. Having a
congenital malformation (i.e. bicuspid aortic valve) is another risk factor

- Clinical manifestation and assessment:

• AS can be asymptomatic for decades. Sx associated w/ AS: angina due to LV hypertrophy &
diminished coronary blood flow; dyspnea due to increased pulmonary venous pressure from LV
failure; & syncope, usually w/o exertion, due to fixed CO.
• On physical exam, a thrill, or a vibration may be felt in the aortic area. The vibration is
caused by turbulent blood flow across the narrowed valve orifice. 
• A loud, systolic ejection murmur (heard on the S1) may be heard over the aortic area, & may
radiate into the neck. This is caused by blood flowing through the narrowed opening of the
stenotic valve. 
• Pt should be instructed to lean forward during auscultation, esp upon exhalation, to
accentuate the murmur. S3 or S4 gallop may be heard.
• Echocardiography is used to dx & monitor progression of AS, & will demonstrate
calcification of the valve or decreased mobility of valve cusps, & LV hypertrophy.
• Pts w/ sx usually have echocardiograms every 6 to 12 months, & those w/o sx have echos
every 2 to 5 yrs. 
• Cardiac catheterization can measure severity of AS when noninvasive testing is
inconclusive.

✦ Aortic regurgitation
- Definition: (aortic insufficiency) is the backward flow of blood into the LV from the aorta
during diastole.

- Pathophysiology:
• When aortic valve is incompetent, blood from the aorta returns to the LV during diastole,
in addition to the blood normally delivered by the left atrium. The LV dilates in an
attempt to accommodate blood volume overload, causing hypertrophy. 
• Dilatation & hypertrophy allow the LV to expel more blood w/ above-normal force, increasing
afterload & as a result, systolic BP, while maintaining a normal ejection fraction. 
• The arteries attempt to compensate for the higher pressures by reflex vasodilation; the
peripheral arterioles relax, reducing peripheral resistance & diastolic BP. 
• Although compensatory mechanisms allow pts to remain asymptomatic despite pressure & volume
overload, when left ventricular dysfunction develops, sx appear.

- Risk factor:
• Calcific valve disease & bicuspid aortic valve are the most common risk factors of AR. B/c
they affect the valve leaflets, rheumatic heart disease and infective endocarditis can
cause AR
• Disorders affecting the aortic root (i.e. Marfan syndrome and dissecting aortic aneurysm,
can lead to AR, as can chronic HTN)

- Clinical manifestation and assessment:

• AR is asymptomatic for yrs, but as it progresses, sx r/t increased stroke volume become
apparent. 
• Palpitations, particularly when lying down, & visible neck vein pulsations are a result of
the increased force & volume of the blood ejected from the hypertrophied LV. 
• Later sx, including dyspnea, fatigue, angina, orthopnea & pulmonary congestion, signify
decreased cardiac reserve, & LV failure. Pulse pressure (difference b/w systolic &
diastolic pressures) widens.
• Another characteristic sign of AR is the water-hammer (Corrigan's) pulse, in which pulse
has a rapid upstroke & collapses. 
• Systolic BP in lower extremities is higher than in the upper extremities. A decrescendo
(gradually decreasing loudness) diastolic murmur (heard on S2) is heard as a high-pitched
blowing sound at 3rd or 4th intercostal space at the left sternal border, heard best w/ pt
sitting up & leaning forward.
• Dx is confirmed by echocardiography; valve morphology, degree of LV hypertrophy, &
functional capacity are determined. Cardiac cath is not necessary in most pts w/ AR. 
• Pts w/ symptoms usually have echocardiograms every 4 to 6 months, & those w/o symptoms have
annual echocardiograms. 
• Exercise stress testing will assess functional capacity & symptom response.

- Surgical and nursing management:

 • No tx is required for asymptomatic pt w/valvular pathology. The goal of medical therapy is
not curative, but it’s symptom relief. Definite therapy for a valvular problem is
mechanical restoration of valve function
• Management is guided by findings on the echocardiogram and is aimed at the specific
valvular problem
• Beta blocker and calcium channel blockers may be used for rate control, to treat
palpitations, for chest discomfort, for anxiety, and useful when there is concomitant
coronary artery disease
• Digoxin is given to increase contractility and slow rapid rates to allow for improved
ventricular filling
• Antiarrhythmics and electrical cardioversion are utilized to restore sinus rhythm, and
anticoagulation is indicated if AF is persistent
• Diuretic, vasodilators, and sodium restriction may be used to reduce preload and pulmonary
congestion
• B/c pt with severe AS are dependent on preload to maintain CO, diuretic should be used with
cautions
• ACE-Is are prescribed to reduce preload, afterload, and HTN by causing vasodilation;
prescribed for pt w/concomitant HTN but may be avoided in pt w/AS b/c vasodilation reduces
pressure distal to the obstruction w/o increasing CO and may cause syncope
• Afterload reduction may be managed with ARBs, nitrates, or hydrazine
• In acute case of decompensation, IV nitroprusside is the vasodilator used most commonly for
afterload reduction, but nitrates should be used with great caution w/AS b/c their use can
result in reduced CO
• Valvular problem increase the pt’s risk developing bacterial endocarditis. Thrombi may
occur on the value leaflet, and they embolize, transient ischemia attacks can occur
• Daily aspirin is recommended for ppl who have had documented TIA, even they are in sinus
rhythm
• Elimination of caffeine and alcohol may control or reduce symptoms and the nurse encourage
the pt to read labels on OTC products (i.e cough medicine

• Assessing valvular heart disorder:

Heart and lung sound are auscultated and peripheral pulses palpated. The nurse assess
the pt with valvular heart disease for S/S of HF, arrhythmias, dizziness, syncope,
weakness, chest pain
Teach the pt about the diagnosis, the progressive nature of valvular disease and tx.
Teach the pt to report any new symptoms or changes in symptoms to PCP
Monitor of sign of activity intolerance, excessive fatigue, palpitations, diaphoresis,
pallor, tachycardia, should be instructed to rest if symptoms occur

✦ Cardiomyopathy:
- Introduction:
• Disorder of the myocardium (heart muscle) a/w mechanical and/or electrical dysfunction.
Both functional & structural abnormalities are present. 
• A functional classification is often used, w/ ventricular dilatation, ventricular
hypertrophy, & restriction being the most common abnormalities. 
• Regardless of cause, cardiomyopathy can lead to severe HF, lethal arrhythmias, & death.
• Nursing management includes assessment for signs of worsening HF, dyspnea, congested lungs,
peripheral edema, & presence of abnormal heart sounds
• All cardiomyopathies result in impaired CO. Decreased stroke volume stimulates the SNS &
the renin-angiotensin-aldosterone response, resulting in increased systemic vascular
resistance & increased sodium & fluid retention, which places an increased workload on the
heart. These alterations lead to HF, myocardial destruction, & death.

- Types: Review Box 16.2 p 482-483

• Dilated cardiomyopathy [DCM] 
• Hypertrophic cardiomyopathy [HCM]
• Restrictive cardiomyopathy
• Arrhythmogenic right ventricular cardiomyopathy [ARVC]
• Stress-induced cardiomyopathy

- Management
- Care after a heart transplant:

- Assistive devices:
• Intra-aortic balloon pump counterpulsation
• Extracorporeal membrane oxygenator
 • Ventricular assist devices
• Total artificial hearts

Infectious cardiac disorders

✦ Rheumatic fever and rheumatic heart disease
- Definition: A systemic inflammatory condition that is a complication of Group A beta-hemolytic
streptococcal (GAS) pharyngitis (strep throat). RF always occur in children and adolescent b/c
of suspected strep throat is treat swiftly with antibiotic

- Pathophysiology:
- Clinical manifestation and assessment:
- Medical and nursing management:

✦ Endocarditis:
- Definition:
• Endocarditis is an infection of the endocardium. Prosthetic heart valves, structural
cardiac defects, & IV drug use account for the majority of IE. 
• Nosocomial (hospital-acquired) infective endocarditis occurs most often in pts w/
bacteremia & an indwelling cath, & in pts who are receiving prolonged IV fluid or
antibiotic therapy. 
• Pts taking immunosuppressive meds or corticosteroids are susceptible to fungal endocarditis

- Pathophysiology:
• Staphylococci & streptococci account for most IE. These pathogens colonize at the site of
an abnormality or injury of the endocardium (i.e., prosthetic valve site)
• Inflammation & infection result in endothelial damage; then platelets, fibrin, blood cells,
& microorganisms cluster as vegetations on the endocardium. The vegetations can embolize to
other tissues throughout the body. 
• Infection may erode through the endocardium into the underlying structures, causing tears
or deformities of valve leaflets, dehiscence of prosthetic valves, deformity of chordae
tendineae, or paravalvular abscesses.
• Acute endocarditis is often caused by Staph infection & its onset is rapid, occurring
within days to wks. Subacute IE, usually caused by Strep, occurs more slowly & its course
is prolonged. 
• Often, onset of endocarditis is insidious, & s/s develop from the infection, destruction of
the heart valves, & embolization of the vegetative growths on the heart. 
• Systemic emboli occur w/ left-sided heart IE; pulmonary emboli can occur when the right
heart is infected, typically from IV drug use.

- Risk factor:
• A cardiac valve w/ epithelial damage will attract bacteria to its surface & this can result
in endocardial infection.
• This injury may be the result of a prosthetic valve; a congenital abnormality, such as a
bicuspid aortic valve; structural abnormality such as MVP; or may be from age-related,
degenerative valvular changes. 
• IV drug use, long-term indwelling catheters & body piercing are also risk factors

- Clinical manifestation and assessment:

• Clinical presentation of IE varies, & dx may be difficult as symptoms are often vague, such
as anorexia, myalgias, fever, chills, weight loss, back & joint pain, & night sweats. 
• Fever is common, but may be intermittent or absent, esp in pts who are receiving
antibiotics or corticosteroids, those who are elderly, or who have heart or renal failure. 
• A heart murmur may be absent initially but develops in almost all pts. Murmurs that worsen
over time are indicative of progressive damage from vegetations or perforation of the valve
or chordae tendineae.
• Osler nodes, Janeway lesions, & Roth spots are distinguishing signs of IE, & are the result
of microembolization. 
• Osler nodes, painful, erythematous nodules, may be present on pads of fingers or toes.
Janeway lesions are painless, red or purple macules found on the palms & soles. Roth spots,
seen on funduscopic exam, are oval retinal hemorrhages w/ pale centers.
• Splinter hemorrhages may be seen under fingernails & toenails, & petechiae may appear on
neck, chest, abdomen, conjunctiva, & mucous membranes. 
• CNS manifestations: HA, transient cerebral ischemia, & strokes, which may be caused by
emboli to the cerebral arteries. 
• Embolization may be a presenting symptom; it may occur at any time & may involve other
organ systems. Cardiomegaly, HF, tachycardia, or splenomegaly may occur.
 • Positive blood cultures are highly sensitive for dx; however, negative blood cultures do
not rule out IE, esp if pt has received antibiotics or if slow-growing bacteria are
present. 
• 3 sets of blood cultures should be obtained before admin of any antimicrobial agents.
• Echo is used widely in dx & can detect presence or absence of vegetations or abscesses,
prosthetic valve dehiscence, new regurgitation, or HF. 
• Other abnormal findings include anemia, elevated WBC counts, elevated erythrocyte
sedimentation rate (ESR), & elevated C-reactive protein. Abnormal ECG findings include
atrioventricular blocks, bundle branch blocks, & fascicular blocks.
- Medical and nursing management:
• Objective of treatment is to eradicate the infection & prevent complications. 
• The cornerstone of treatment is LT parenteral antibiotic therapy. It is administered in
doses that produce a high serum concentration & for a significant period, often for upward
of 6 wks to ensure eradication of the dormant bacteria within the dense vegetations.
• Surgery is indicated when there is a persistent or recurrent infection, if HF occurs, or if
pts have more than 1 serious systemic embolic episode, valve obstruction, valvular or
myocardial abscess, or fungal endocarditis. 
• Most pts who have prosthetic valve endocarditis require valve replacement, & this greatly
improves the prognosis for pts w/ severe symptoms. 
• Nurse monitors pt for fever, which can persist for wks. Heart sounds are assessed. A new or
worsening murmur may indicate dehiscence of a prosthetic valve, rupture of an abscess, or
injury to valve leaflets. 
• Nurse monitors for s/s of systemic embolization, & end-organ damage that may result, such
as cerebrovascular accident, meningitis, HF, MI, pulmonary embolism, glomerulonephritis, &
splenomegaly.
• Pt care is directed toward management of infection. Antibiotics are initiated as soon as
blood cultures have been obtained. Long-term IV antimicrobial therapy is often necessary, &
many pts have PICCs or other long-term IV access. 
• All invasive lines & wounds must be assessed daily for redness, tenderness, warmth,
swelling, drainage, or other signs of infection.
• Nurse instructs the highest-risk pts & fam about the need for prophylactic antibiotics
before certain dental procedures.
• For pts w/ low to moderate risk of developing IE, esp those who have previously received
antibiotic prophylaxis, education must be provided regarding the updated recommendations.
• Rationale (Box 16-4) must be provided for no longer providing prophylaxis for GU & GI
procedures, as well as for most resp & dental procedures, except in highest-risk
individuals.
• Blood cultures are taken periodically to monitor effect of therapy, & serum lvls of
selected antibiotic are monitored to ensure the serum demonstrates bactericidal activity.
• If pt has undergone surgical treatment, nurse provides postop care & instructions.

✦ Myocarditis:
- Definition:
• Inflammation of the heart muscle, commonly resulting from viral infection. It may also be
caused by bacterial infections, immune-mediated mechanisms, & toxic agents. Freq cause is
unknown.
• Can be acute or chronic. Mortality varies w/ the severity of symptoms. Mild cases w/ few
symptoms may resolve w/o treatment, while more serious cases result in cardiogenic shock &
death.

- Pathophysiology:
• Cardiac muscle inflammation that results in myocyte necrosis is the hallmark of
myocarditis. 
• Acute myocarditis is characterized by myocyte damage from viral infection, autoimmunity, or
other precipitating event. Myocyte antigens & cytokines are released. In the subacute phase
(days 4 to 14), T & B lymphocytes infiltrate the myocardium, & the virus is cleared. The
immune response continues & infected myocytes are lysed.
• During the chronic phase, myocyte injury continues & can lead to dilated cardiomyopathy.

- Clinical manifestation and assessment:

• Sx depend on the type of infection, degree of myocardial damage, & capacity of the
myocardium to recover. Dx is difficult. 
• Clinical presentation can vary widely; symptoms can range from mild systemic findings of
fever, myalgias, fatigue, & dyspnea to ventricular arrhythmias, cardiogenic shock, & DCM. 
• Other s/s: S3 gallop, tachycardia, tachypnea, JVD, edema, ECG abnormalities, orthopnea, &
palpitations. 
 • Fulminant HF or sudden cardiac death can quickly develop
• A minority will have elevated cardiac enzymes & WBC count. ESR will be elevated approx 60%
of the time. 
• Echocardiography may show impaired heart muscle function or pericardial effusion.
Myocardial biopsy may be used to confirm dx.

- Medical and nursing management:

• For pts w/ myocarditis, supportive care is of primary importance, w/ goals of care focused
on maintaining hemodynamic stability & improvement of symptoms.
• Treatment of HF symptoms w/ standard medical therapy & surgical options, such as placement
of a VAD or TAH, or heart transplantation, should be considered when there is no
improvement in symptoms or hemodynamic status despite maximal medical therapy.
• Nursing care of pt w/ myocarditis includes an assessment of whether the pt's symptoms are
improving or worsening.
• In addition to monitoring vital signs, heart sounds, lung sounds, & peripheral perfusion,
nurse must assess hemodynamic, oxygenation, & fluid status. 
• Nurses should be prepared to use emergency equipment, as risk of life-threatening
ventricular arrhythmias is great. 
• Nurses must also provide emotional support to pt & fam; myocarditis can be particularly
stressful due to its variable presentation & course.

✦ Pericarditis:
- Definition:
• Inflammation of the pericardium (membranous sac surrounding the heart) 
• Causes are numerous, but it is most freq caused by viral illness, & may also occur
following certain medical problems or after some surgical procedures.
• Pericarditis can develop after an acute MI or following pericardectomy (opening of the
pericardium) during cardiac surgery.

- Pathophysiology:
• Pericardial sac consists of 2 layers: parietal (outer) layer & visceral (inner) layer that
is affixed to the heart. 
• A small amount of fluid (15 to 50 mL) separates the layers. Pericarditis may lead to an
accumulation of fluid in this space (pericardial effusion). This may result in increased
pressure on the heart, leading to cardiac tamponade.
• Pericarditis may be acute or chronic. Acute develops rapidly, causing an inflammatory
reaction, while chronic progresses slowly & can be accompanied by effusion
• Freq or prolonged episodes of pericarditis can lead to thickening & decreased elasticity of
the pericardium, & scarring may fuse the visceral & parietal pericardium.
• These conditions restrict the heart's ability to fill w/ blood (constrictive pericarditis).
The pericardium may become calcified, further restricting ventricular expansion during
diastole. 
• W/ less filling, the ventricles pump less blood, leading to decreased CO & s/s of HF.
Restricted diastolic filling may result in increased systemic venous pressure, causing
peripheral edema & hepatic failure.

- Risk factor:
• Men b/w ages of 20 & 50 are more likely to develop pericarditis. 
• It can occur following a MI or recent viral illness or bacterial infection. Lupus,
scleroderma, rheumatoid arthritis, or other autoimmune disorders are risk factors for the
development of pericarditis. In about half of all cases, the cause is unknown (idiopathic).

- Clinical manifestation and assessment:

• Pericarditis may be asymptomatic; however, the most characteristic symptom is chest pain.
• B/c of this & ST-segment elevation that is often present, acute pericarditis can mimic
acute MI. The pain is typically persistent, sharp, pleuritic, & usually felt in the mid-
chest, although it also may be located beneath the clavicle, in the neck, or in the left
trapezius region. 
• The discomfort is usually fairly constant, but is aggravated by deep inspiration, coughing,
lying down, or turning. It may be relieved w/ a forward-leaning or sitting position. 
• Although not heard in all pts w/ pericarditis, a common finding is a creaky or scratchy
friction rub.
• Other signs may include a mild fever, increased WBC count, anemia, & an elevated ESR or C-
reactive protein lvl. Pts may have a nonproductive cough. Dyspnea unrelated to exertion is
typical; shortness of breath occurs as a result of pericardial compression due from cardiac
tamponade.
 • Dx most often made on the basis of the history, signs, & symptoms. A 12-lead ECG may show
diffuse concave ST elevation w/o reciprocal changes or T-wave inversion, & ST-segment
elevation may persist for wks. ECG may also reveal depressed PR segments or atrial
arrhythmias. Echocardiography done to assess for pericardial effusion or tamponade.

- Medical and nursing assessment:

• Goals of management are to determine the cause, administer therapy for treatment & symptom
relief, & detect s/s of cardiac tamponade. 
• NSAIDs are prescribed for pain relief during acute phase. Corticosteroids may be prescribed
if pericarditis is severe or if pt does not respond to NSAIDs. 
• Corticosteroids & NSAIDs, however, should not be given to pts who develop pericarditis
following an acute MI b/c they can cause rupture of the infarcted area. 
• In cases of constrictive pericarditis, surgical removal of the pericardium (pericardectomy)
may be necessary to provide relief from restrictive inflammation& scarring.
• Pts w/ acute pericarditis require pain management w/ analgesics, positioning, &
psychological support. Pts w/ chest pain often benefit from education & reassurance that
the pain is not a heart attack.
• Nurse monitors pt for HF, & treats pts w/ hemodynamic instability or pulmonary congestion
as if they had HF.

Questions
✦ A patient has just begun treatment for endocarditis. The patient’s treatment plan would be
primarily based on the results of which of the following diagnostic tests?
A. Ultrasound of the heart
B. Blood cultures
C. ABGs
D. CBC
 Arrhythmias and Conduction Problems (p.497-529)
✦ What are arrhythmias/dysrhythmias? disorders of the electrical impulse within the heart that cause
disturbances of HR , heart rhythm, or both
- W/o normal rate & regular rhythm, the heart does not perform efficiently as a pump to circulate
oxygenated blood
- Produce symptoms R/T to the hemodynamic effect they cause (i.e. decrease in cardiac output,
increase the risk of clot formation within the chambers of the heart)
- Arrhythmias named according to the site of origin of the impulse (i.e. atria or ventricle) and
the mechanism of formation or conduction involved (i.e. bradycardia, tachycardia, premature)
- Their presence is confirmed by an ECG

System Signs and symptoms of decreased cardiac output

Respiratory Tachypnea, SOB, orthopnea, dyspnea on exertion, hypoxemia, crackles on lung

auscultation, wheeze, dry or productive cough

Cardiac and Edema, jugular vein distention, displaced point of maximum impulse, S3 gallop
peripheral vascular rhythm, tricuspid and/or mitral regurgitation murmurs, hypotension, decreased mean
arterial pressure, narrow pulse pressure, cool skin and extremities, delayed
capillary refill, tachycardia

Renal Decreased urinary output, oliguria, rising creatinine

Gastrointestinal Abdominal distention, ascites, liver engorgement, positive abdominojugular refelx

Central nervous Dizziness, decreased sensorium, syncope, fatigue

Behavioral/emotional Anxiety, restlessness

✦ Electrocardiogram (ECG)
- The electrical impulse that travels through the heart
- Each phase of the cardiac cycle is reflected by specific waveforms. The number & placement of
the electrodes used depend on type of ECG needed
- The electrodes record waveforms that appears on the paper or monitor and represent the
electrical current in relation to 2 electrodes
- HR and rhythm monitored effectively through only 2 electrodes. However, the use of 10
electrodes (resulting in 12 leads) provides more detailed info and is the basis for
understanding other types of ECG monitoring

✦ The 12-Lead ECG

- A diagnostic tool that uses 10 electrodes: one placed on each limb and six placed on the chest
(precordial) produce 12 different waveforms/leads
- Include three bipolar leads (I, II, III) and nine unipolar leads (aVR, aVL, aVF, V1-V0)
• Bipolar leads measure electrical activity traveling between a positive and negative electrode
• Unipolar leads record electrical activity from a single reference point
• Together they show electrical activity in both a frontal plane and a transverse plane
• When viewed together, these two planes provide diagnostic info: HR, rhythm, conduction
abnormalities (i.e. bundle branch block), heart chamber enlargement, localization of ischemia
or infarction, noncardiac condition (i.e. electrolyte imbalances caused by hypocalcemia,
hyperkalemia, or hypomagnesium
- Electrode placement for a 12-lead ECG must be accurate and consistent as misplacement can
result in altered waveforms, which can lead to inaccurate diagnosis and treatment. Electrode
placement is important in arrhythmia identification & is crucial in identifying changes related
to ischemia, infarction, & many arrhythmias.
- The 4 limb electrodes are placed on the lower legs, near the ankles, & on the arms, near the
wrists; The remaining 6 electrodes are placed across the left side of the chest. Locating the
specific anatomical landmark is critical for correct chest electrode placement
- If the pt needs a series of ECGs, consistency of electrode placement is also important. In some
cases, the chest electrodes are left in place or the correct location is marked w/ an indelible
pen to ensure the identical placement for follow-up ECGs

✦ Interpreting the ECG:

- ECG waveforms are printed on graph paper that is divided by light & dark vertical & horizontal
lines at standard intervals; Time & rate are measured on horizontal axis of graph, & amplitude
or voltage is measured on vertical axis
 - Each small block on the graph paper equals 0.04 second, & 5 small blocks form a large block,
which equals 0.2 second
- When an ECG waveform moves toward the top of the paper, it is called a positive deflection;
When it moves toward the bottom of the paper, it is called a negative deflection
- The ECG is composed of waveforms (including P wave, QRS complex, T wave, & possibly a U wave) &
of segments or intervals (PR interval, ST segment, & QT interval)

✦ ECG waveforms (Waves):

- P wave: represents the electrical impulse starting in the sinus node & spreading through the
atria (atrial depolarization leading to atrial contraction)
- QRS Complex: represents ventricular depolarization; Not all QRS complexes have all 3 waveforms
(Q wave is the first negative deflection after the P wave; R wave is first positive deflection
after P wave; S wave is first negative deflection after R wave); This complex is normally less
than 0.10 seconds in duration (2.5 small boxes)
- T wave: represents ventricular repolarization or electrical recovery; Follows QRS complex & is
usually in same direction as QRS complex; Atrial reploarization also occurs but is not visible
on ECG b/c it occurs at same time as QRS
- U wave: may or may not b present; thought to represent depolarization of Purkinje fibers; is
sometimes seen in pts w/ hypokalemia, hypertension, or heart disease; If present, U wave
follows T wave & usually smaller than P wave--if tall, it may be mistaken for an extra P wave

✦ ECG waveforms (interval and segments)

- PR interval: measures from beginning of P wave to beginning of QRS complex & represents time
needed for sinus node stimulation, atrial depolarization, & conduction through AV node before
ventricle depolarization; Normal range for PR is 0.12-0.20 seconds
- ST segment: represents early ventricular depolarization, lasts from end of QRS complex to
beginning of T wave; beginning of ST segment is usually identified by change in thickness or
angle of terminal portion of the QRS complex & is called the J point; end of ST segment may be
more difficult to identify b/c it merges into the T wave; St segment is analyzed to identify
whether it is above or below isoelectric line (baseline or flat part of ECG), which may be,
among other s/s, a sign of cardiac ischemia
- QT interval: represents total time for ventricular depolarization & depolarization; measured
from beginning of QRS complex to end of T wave; varies w/ HR, gender, & age; If QT interval
becomes prolonged, pt may be at risk for lethal ventricular arrhythmia called torsades de
pointes; corrected Qt (QTc) is calculated based on HR & is more determinant of risk for
torsades de pointes arrhythmia; Nurse should measures QT interval every 8-12 hrs & calculate
Qtc on printouts of rhythm strips from bedside or telemetry monitor for pts at risk for
torsades de pointes; QTc > 0.47 second for males or > 0.48 second for females is indicative of
increased risk for torsades de pointes, & QTc > 0.50 second is considered dangerously prolonged
- Nurses should note: ST segment depression seen w/ ischemia; ST segment elevation seen w/
injury; Q waves seen w/ necrosis & infarction
- PP & RR intervals ar measured from beginning of 1 P or R wave to the beginning of the next P or
R wave; PP interval is used to determine atrial rate & rhythm; RR interval is measured from 1
QRS complex to the next QRS complex; RR interval is used to determine ventricular rate & rhythm

Cardiac rhythms
✦ Normal sinus rhythm: Box 17-4 and Figure 17-5
- Normal sinus rhythm occurs when the electrical impulse starts at the sinus node & travels
through the normal conduction pathway; Serves as a baseline for comparison in identifying all
other arrythmias
- ECG characteristics: Rate (60-100 in the adult); Rhythm (regular); P wave (normal & consistent
shape; always in front of QRS); PR interval (consistent interval b/w 0.12-0.20 seconds); QRS
duration (less than 0.10 seconds)

Abnormal sinus rhythms

✦ Sinus bradycardia:
- Pathophysiology:
• Occurs when the sinus node creates an impulse at a slower-than-normal rate
• Causes include: lower metabolic needs (e.g. sleep, athletic training, hypothyroidism),
vagal stimulation (e.g. from vomiting, suctioning, servere pain, extreme emotions),
medications (e.g. calcium channel blockers, amiodarone, beta blockers), increased
intracranial pressure, & myocardial infraction

- Clinical manifestation and assessment:

• Sinus bradycardia often does not cause symptoms
 • The pt is assessed to determine the hemodynamic effect, if any, & the possible cause of the
arrhythmia
• ECG characteristics are: Rate (Less than 60 bpm); Rhythm (Regular); P wave (Present before
each QRS & consistent in size & shape); PR interval (Normal); QRS duration (Normal)

- Medical and nursing management:

• Only bradycardias that cause serious s/s (altered mental status, ongoing chest pain,
hypotension, or shock) require immediate treatmen
• Treatment of symptomatic bradycardia includes: transcutaneous pacing & atropine; If pacing
is unavailable or ineffective, a dopamine or epinephrine infusion may be considere
• If significant bradycardia is due to meds, they should be held, & their necessity is
reevaluated

✦ Sinus tachycardia:
- Pathophysiology:
• Sinus tachycardia occurs when the sinus node creates an impulse at a faster-than-normal rat
• Causes include: physiologic or psychological stress (e.g. acute blood loss, anemia, shock,
hypervolemia, hypovolemia, HF, pain, hyper metabolic states, fever, exercise, anxiety);
Medications that stimulate sympathetic response (e.g. catecholamines, aminophylline,
atropine), stimulants ( e.g. caffeine, alcohol, nicotine), & illicit drugs (e.g.
amphetamines, cocaine, Ecstasy)

- Clinical manifestation and assessment:

• Sinus tachycardia often does not cause symptom
• As the HR increases, the diastolic filling time decreases, possibly resulting in reduced CO
& associated symptoms
• If the rapid rate persists & the heart can no longer compensate for the decreased
ventricular filling, the pt may develop acute pulmonary edema or cardiac ischemia
• ECG characteristics are: Rate (Greater than 100 bpm); Rhythm (Regular); P wave (Present
before each QRS & consistent in size & shape) PR interval (Normal) QRS duration (Normal)

- Medical and nursing management:

• Treatment of sinus tachycardia is usually determined by the severity of symptoms & directed
at identifying & treating its cause
• For example, tachycardia caused by acute blood loss would be treated w/ IV fluid
replacement & blood transfusion

✦ Premature atrial complex

- Pathophysiology: PAC is a single ECG complex that occurs when an electrical impulse starts in
the atrium before the next normal impulse of the sinus node
• Caused by caffeine alcohol, nicotine, stretched atrial myocardium (i.e. hypervolemia),
anxiety, hypokalemia (low K+ level), hyper metabolic states (i.e. with pregnancy), hypoxemia,
or atrial ischemia, injury, or infarction
- Clinical manifestation and Assessment:
• PACs are common ECG findings, found w/o cardiac pathology, asymptomatic
• ECG characteristics are:
Rate: depends on the underlying rhythm
Rhythm: Irregular
P wave: Size and shape of the P wave associated w/premature beat is different from sinus
node-generated P wave
PR interval: The PR interval of the premature beat is greater than 0.12 sec but shorter
than the sinus generated PR interval
QRS duration: Normal
- Medical and Nursing assessment:
• PACs is infrequent, no treatment is necessary since hemodynamic stability is maintained
• If they are frequent (more than 6 per min), could be a sign of a worsening condition or the
onset of more serious arrhythmias (i.e. AF) and further work-up may be clinically indicated

✦ Atrial flutter “sawtooth”

- Pathophysiology: Occurs in the atrium and creates impulses at a rapid but regular atrial rate
btwn 220-350 times per min
• Atrial rate is faster than the atrioventricular (AV) node can conduct

✦ Atrial fibrillation (can be intermittent or chronic)

- Pathophysiology:
 • Atrial fibrillation causes a rapid, disorganized, & uncoordinated electrical activity
within the atria
• May be transient, starting & stopping suddenly & occurring for a very short time
(paroxysmal), OR is may be persistent, requiring treatment to terminate the rhythm or to
control ventricular rate
• The erratic atrial contraction promotes formation of thrombi within the atria, increasing
risk for an embolic event like stroke
• Atrial fibrillation is usually associated w/ advanced age, valvular heart disease, CAD,
hypertension, HF, cardiomyopathy, diabetes, hyperthyroidism, pulmonary disease, chronic
lung disease, & surgery (esp open heart surgery)
• Physiological stressors like hypoxia, infection, & hypoglycemia, as well as caffeine &
sympathomimetic drugs are also associated w/ atrial fibrillation
• Sometimes atrial fibrillation occurs in people w/o any underlying pathophysiology

- Clinical manifestation and assessment:

• People w/ a. fib. may be asymptomatic
• A rapid ventricular response reduces the time for ventricular filling, resulting in a
smaller stroke volume; Additionally, loss of atrial contraction (sometimes referred to as
atrial kick) reduces ventricular filling volume & reduces CO by 25%--This leads to symptoms
of fatigue & malaise
• The shorter time in diastole reduces the time available for coronary artery perfusion,
thereby increasing risk for myocardial ischemia
• ECG characteristics are: Rate (Atrial rate is 300 -400, w/ a variable ventricular response
rate (typically rapid)); Rhythm (Irregular); P wave (No discernible P waves; irregular
undulating waves may be seen & are referred to as fibrillatory waves); PR interval (Not
measurable); QRS duration (Normal)

- Medical and nursing management:

• Treatment of a.fib. depends on its cause & duration & the pt's symptoms, age, &
comorbidities
• The management of a.fib. includes: controlling ventricular rate & achieving rhythm
conversion to sinus rhythm if possible; Electrical cardioversion is indicated for a.fib.
that is hemodynamically unstable 
• B/c of high risk for embolization of atrial thrombi, cardioversion of a.fib. that has
lasted longer than 48 hrs should be avoided unless pt has received anticoagulants
• For a.fib. of acute onset (usually defined as that w/ an onset within 48 hrs), IV adenosine
(Adenocard) has been used to achieve cardioversion to sinus rhythm as well as to assist in
the dx
• Warfarin is indicated if pt w/ a.fib. is at high risk for stroke (e.g. >75 or has
hypertension, diabetes, HF, or hx of stroke)
• If immediate anticoagulation is necessary, pt may be placed on heparin until the warfarin
lvl is therapeutic
• Pacemaker implantation or catheter ablation is sometimes indicated for pts who are
unresponsive to meds
• Catheter ablation is an invasive procedure during which high-frequency radio waves are
applied to destroy tissue at site of arrhythmia; Ablation procedures are usually performed
in electrophysiologic labs & are similar to other types of heart catheterization--During a
catheter ablation, long, thin, flexible tubes are placed in heart via vascular system; A
diagnostic catheter determines where the abnormal tissue that is causing the arrhythmia is
located; High-frequency energy is sent into the tissue, creating a lesion or scar; The area
is now ablated (destroyed), thus facilitating normal electrical conduction
• Several approaches are effective in preventing occurrence of postoperative a.fib.,
including preoperative admin of a beta blocker or immediate postoperative admin of IV
amiodarone

Questions
✦ Which of the following arrhythmias creates the most significant risk for cerebrovascular (stroke)
accident?
A. Sinus tachycardia
B. Sinus bradycardia
C. Atrial fibrillation
D. Premature atrial complex

Abnormal ventricular rhythms

✦ Ventricular arrhythmias
✦ Ventricular tachycardia:
 - Pathophysiology:
• Ventricular tachycardia is defined as 3 or more consecutive ventricular beats, occurring at
a rate exceeding 100 bpm
• Causes: intake of caffeine, nicotine, or alcohol; cardiac ischemia or infarction; increased
workload on heart (e.g. exercise, fever, hypervolemia, HF); digitalis toxicity, hypoxia,
acidosis, or electrolyte imbalances (esp hypokalemia)
• Usually associated w/ CAD & may precede ventricular fibrillation
• Untreated ventricular tachycardia can deteriorate into ventricular fibrillation, a lethal
arrhythmia

- Clinical manifestation and assessment:

• The pt can experience a range of symptoms related to decreased CO, such as hypotension or
syncope, pulselessness, & unresponsiveness
• Some pts may be asymptomatic
• ECG characteristics are: Rate (100-250 bpm); Rhythm (Regular); P wave (Usually not visible;
if visible are not associated w/ QRS complex (called dissociation)); PR interval (None);
QRS duration (Greater than 0.12 seconds)

✦ Ventricular fibrillation:
- Pathophysiology:
• Ventricular Fibrillation: rapid, disorganized rhythm that causes ineffective quivering of
the ventricles
• No atrial activity is seen on ECG
• Causes: same as for ventricular tachycardia; may also result from untreated or
unsuccessfully treated ventricular tachycardia

- Clinical manifestation and assessment:

• Clinical manifestations include: absence of an audible heartbeat, a palpable pulse, &
respirations; Cardiac arrest & death are imminen
• ECG characteristics are: Rate (Often cannot be determined, but is greater than 220 bpm);
Rhythm (Irregular); P wave (Not visible); PR interval (Not visible); QRS duration (Not
visible)

✦ Ventricular systole

Atrioventricular (AV) heart blocks

✦ First-degree AV block
- Occurs when atrial conduction is delayed through AV node, resulting in a prolonged PR interval
- Pathophysiology:
• Occur w/o an underlying pathophysiology or may be the result of meds (i.e. beta blockers,
calcium-channel blockers, digoxin).
• It can result from conditions that increase parasympathetic (vagal) tone (i.e. vomiting or
Valsalva maneuver)
- Clinical manifestations and assessment:
• The patient is usually asymptomatic:
Rate: depends on underlying rhythm
Rhythm: Regular
P wave: Present before each QRS and consistent in size and shape
PR interval: Greater than 0.20 secs
QRS duration: Normal
- Medical and nursing management:
Only treated if symptoms R/T bradycardia are present
If the AV block is new, the pt should be observed for potential progression to second-
degree block
No treatment for it

✦ 2nd degree AV block, Type 1 (Wenckebach)

- Occurs when there is a repeating pattern in which all but one of a series of atrial impulses
are conducted through AV node into the ventricles (i.e. every 4 of 5 atrial impulses are not
conducted)
- Each atrial impulses take a longer time for conduction than the one before, until one impulse
is fully blocked, an increasing PR interval is seen with each successive beat until a P wave is
seen w/o a resulting QRS
- AV node is not depolarized by the blocked atrial impulse, AV node has time to fully depolarize
so that the next atrial impulse can be conducted within the shortest amt of time
- Pathophysiology:
 • Caused by a gradual and progressive conduction delay through AV node. Can be R/T increased
parasympathetic (vagal) tone, ischemia, or meds that slow conduction (i.e. beta blockers,
calcium-channel blockers, digoxin)
- Clinical manifestation and assessment:
• R/T bradycardia and include chest discomfort, dyspnea, hypotension
• ECG characteristics:
Rate: Atrial rate faster than ventricular rate
Rhythm: The atrial rhythm is usually regular, the ventricular rhythm is usually irregular
P wave: Size and shape normal
PR interval: Pr interval becomes longer with each succeeding ECG complex until there is a
P wave not followed by a QRS
QRS duration: normal
- Medical and nursing management:
IF pt has symptomatic bradycardia, treatment w/atropine (if the rate drops) or
transcutaneous pacing is indicated

✦ 3rd degree AV block

Arrhythmias and Conduction Problems

✦ Nursing assessment
- Obtain a health history to identify:
• any previous occurrences of possible decreased CO (i.e. near-syncope, fainting, light-
headedness, dizziness, fatigue, chest discomfort, SOB, palpitations)
• Comorbidities or coexisting conditions that could be a possible cause of the arrhythmia (i.e.
heart disease, COPD, pre-existing thyroid disease, Lyme disease)
• All medications (prescribed and OTC)
• Lab results are reviewed to assess levels of meds
- A psychosocial assessment is performed to identify possible effects of the arrhythmias, the
pt’s perception of the arrhythmia, and whether anxiety is a significant contributing factor
- Assess the pt’s skin (i.e. pale and cool), sign of fluid retention
✦ Nursing interventions
✦ Treatments
- Cardioversion for atrial abnormal rhythm (dysrhythmias or arrhythmias)
 Exam 3: Vascular disorders
Peripheral arterial disease
❖ Forms of PAD
❖ Risk factors
❖ Clinical signs and symptoms
❖ Treatment
❖ Post-operative care

Question
❖ A pt report experiencing pain in the left lower leg and foot when walking. This pain is relieved
with rest. The nurse should suspect that this pt has which of the following?
A. Coronary
B. Intermitten
Aneurysm
❖ What is an aneurysm?
❖ Risk factor: tobacco use, high blood pressure, elderly , genetic
❖ Common types
❖ Signs
❖ Treatment
❖ Nursing management: manage blood pressure, monitor BP,

Venous thrombosis (DVT)

❖ Virchow triad
❖ Medical management
❖ Nursing management

Varicose veins
❖ Risk factors
❖ Prevention
❖ Surgical treatments

Vascular ulcers
❖ Ulcer types
❖ Treatment
❖ Wound care

Lymphatic disorders
❖ Lymphangitis
❖ Lymphedema