NCM102 - Cardio2

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V Hypertension
Etiology and Pathophysiology
Hypertension increases the risk of coronary artery
disease, heart failure, MI, CVA and renal failure
Risk Factors include: Stress, obesity, nutrition (high
Na, low Ca, Mg and K), substance abuse (cigarettes,
alcohol, cocaine), Family history, age, sedantary
lifestyle, hyperlipidemia.
Often asymptomatic; Dx requires three assessments
of elevated BP on separate occassions.

V Hypertension
Classification of BP
Optimal: systolic <129mm Hg; diastolic <80 mm Hg
Normal: systolic <130mm Hg; diastolic <85mm Hg
High normal: systolic 130 to 139 mm Hg; diastolic 85 to 89
mm Hg
Hypertension: stage 1: systolic 140 to 159 mm Hg, diastolic
90 to 99 mm Hg; stage 2: systolic 160 to 179 mm Hg,
diastolic 100 to 109 mm Hg; stage 3: systolic 180 mm Hg,
diastolic 110 mm Hg
V Hypertension
Primary (essential) hypertension
90 to 95% of all cases of hypertension
Etiology is complex; begins insidiuosly; changes in

arteriolar bed cause increased resistance; increased
blood volume may result from hormonal or renal
dysfunction; arteriolar thickening causes increased
resistance; increased blood volume may result from
hormonal or renal dysfunction; arteriolar thickening
causes increased peripheral vascular resistance;
anbormal renin release constricts arterioles.
V Hypertension
Secondary hypertension
Results from renovascular disease;
hyperaldosteronism; Cushingǯs syndrome; DM;
dysfunction of thyroid, pituitary or parathyroid
glands; coarctation of the aorta and pregnancy.
V Hypertension
Clinical Findings:
Subjective: headache (occipital area);
lightheadedness; tinnitus; easy fatigue; visual
disturbances; palpitations.
Objective: BP greater than 140/90 mm Hg obtained
on 3 separate occasions; retinal changes; renal

pathology (azotemia); epistaxis; cardiac
hypertrophy.
V Hypertension
Therapeutic Interventions
Lifestyle modifications; sodium restriction (1 to 2 g
daily); weight control or reduction; alcohol
restriction; cessation of smoking; regular exercise
program ; stress management.
Diuretics, Beta blocker, calcium antagonist, ACE
inhibitors is prescribed based on clientǯs other
health problems.
V Hypertension
If ineffective, the dosage of the drug is increased, a
different drug is given or a second drug of a different
classification is added.
If still ineffective a second drug is substituted or a
third drug of a different classification is added.

If still ineffective a third or fourth drug is added.
Relaxation modalities such as biofeedback and
guided imagery.
V Hypertension
Nursing care of client with HPN
Assessment:
VS with client in both upright and recumbent
positions; baseline weight; presence of risk factors
and clinical findings.
Nursing diagnoses
Imbalanced nutrition: more than body requirements
r/t lack of knowledge of relationship between diet
and disease process
V Hypertension
Nursing diagnosis
Ineffective health maintenance r/t deficient
knowledge regarding treatment and control of
disease process
Fear r/t questionable prognosis and potential
disability or death
V Hypertension
Planning/ Implementation
Monitor electrolytes, BUN, creatinine, lipid profile
and proteinuria
Weigh client daily when there is threat of heart
failure
Teach client to monitor own BP; advise client to
change position slowly and avoid hot showers to
prevent orthostatic hypotension
Reinforce that hypertension is not cured but
controlled
V Hypertension
Planning/ Implementation
Reassure and support any expression of emotions;
encourage relaxation techniques.
Educate the client and family regarding drugs, follow
up care, activity restrictions and diet.
V Coronary Artery Disease (CAD): Atherosclerosis,
Angina Pectoris, Myocardial Infarction
Atherosclerosis: deposition of fatty plaques along
inner wall of coronary arteries leads to smooth
muscle cell proliferation, narrowing and possible
obstruction; also affects peripheral and cerebral
vessels.
Angina pectoris: episodic pain experienced when
oxygen supplied by the blood cannot meet the
metabolic demands of the muscle.
V TYPES OF ANGINA PECTORIS
V Stable Angina
Chest pain lasts for less than 15 minutes
Recurrence is less frequent
V Unstable Angina (Preinfarction Angina, Crescendo Angina,

Intermittent Coronary Syndrome)
Chest pain last for more than 15 minutes but less than 30 minutes
Recurrence is more frequent, may occur at night
Intensity of pain increases
V Variant Angina (Prinzmetalǯs Angina)

Chest pain is of longer duration and may occur at rest
The attacks tend to occur in the early hours of the day
May result from coronary artery spasm
V Nocturnal Angina
Occurs only during the night and is possibly associated
with rapid eye movement (REM) sleep
V Angina Decubitus
Paroxysmal chest pain that occurs when the client sits
or stands up
V Intractable Angina
Chronic, incapacitating angina unresponsive to
intervention
V Postinfarction Angina
Occurs after MI, when residual ischemia may cause
episodes of angina
Myocardial infarction (MI): Acute necrosis of the
heart muscle caused by interruption of O2 supply to
the are, resulting in altered function and reduced
cardiac output.
Risk factors:
Family history, increasing age, gender; males and females
especially after menopause, race: higher in african-
americans, cigarette smoking, hypertension,
hyperlipidemia, obesity, sedentary lifestyle, diabetes, stress
Clinical Findings
Subjective: retrosternal chest pain: pain may radiate
to arms, jaw, neck, shoulder or back; pain described
as Ǯpressureǯ, Ǯcrushingǯ or Ǯviselikeǯ; pain of angina is
associated with activity and generally subsides with
rest; palpitations; apprehension, feeling of dread;
dyspnea, nausea; asymptomatic with silent ischemia.
Clinical Findings
Objective:
ECG changes may reveal ischemia (inverted T wave,
elevated ST segment) or evidence of MI (presence of Q
wave)
Elevated serum enzymes and isoenzymes with MI: cardiac
troponin T levels increase within 3 to 6 hours and remain
elevated 14 to 21 days
Cardiac troponin I levels rise 7 to 14 hours after an MI and
remain elevated for 5 to 7 days
Clinical Findings
Objective:
Creatinine Kinase or Creatinine Phosphokinase elevated 3
to 6 hours after infarction, peaking at 24 hours and
returning to normal within 72 to 96 hours.
CK-MB elevated 4 to 6 hours after pain, peaking within 24
hours
LDH elevated on first day and reaches its peak on third to
fourth day
Clinical Findings
Objective:
Aspartate aminotransferase (AST) elevated on days 2 to 4
Prevention of MI:
Supervised exercise program to avoid ischemia but
promote collateral circulation, increase HDL; weight
control; smoking cessation; dietary restriction of
cholesterol and saturated fat.
Prevention of MI:
Pharmacologic management; nitrates, beta-blocking
agents, calcium channel-blocking agents,
antilipidemics, antiplatelet agents.
Supplemental oxygen during anginal attack as
needed
PTCA
CABG if medical regimen not successful

Intracoronary stent placement
Management of acute MI
Improvement of perfusion: administer ASA
immediately en route to hospital; begin beta blockers
and IV nitroglycerin; thrombolytic therapy within 3
to 6 hours of MI; antidysrhythmics to maintain
cardiac function.
Promotion of comfort and rest: administer analgesics
such as IV morphine sulfate; O2 administration to
alter tissue hypoxia; Maintain bed rest to decrease
oxygen tissue demands.
Monitor client; pulse oximetry, cardiac monitoring,
VS monitoring
Assessment for complications of MI: shock,
pulmonary edema, embolism, pericarditis
Nursing care:
Assessment: History of chest, arm, shoulder, neck,
jaw pain, precipitating factors, risk factors, vital
signs, intake and output, adventitious breath sounds
and dependent edema, restlessness, dyspnea,
diaphoresis, pallor, cyanosis, if MI is suspected
continuous ECG monitoring to detect changes in rate,
rhythm and conduction of heartbeat.
Nursing care:
Nursing Diagnoses:
Acute pain r/t myocardial tissue damage from
inadequate blood supply
Decreased cardiac output r/t ventricular damage,
ischemia, dysrhythmias
Ineffective sexuality patterns r/t fear of chest pain,
possibility of heart damage

Planning / Implementation:
Teach signs and management of cardiac ischemia
(rest, nitrates, emergency care if needed)
Encourage prophylactic administration of nitrates
Reinforce need to avoid nonaerobic exertion and

exposure to cold air
Low cholesterol, low fat diet; eat fish high in omega-
3 fatty acids, increase intake of high-fiber foods

Planning / Implementation:
Provide emotional support regarding alteration in
lifestyle
Support involvement in smoking cessation programs
V Heart Failure
Inability of the heart to meet the demands of the
body.
Pump failure may be caused by cardiac
abnormalities or conditions that place increased
demands on the heart such as cardiac muscle
disorders, valvular disorders, hypertension, coronary
atherosclerosis, hyperthyroidism, obesity
When one side fails there is a buildup in the vascular
system feeding into that side.

V Heart Failure
Right ventricular failure will be evident in the
systemic circulation, those of left-ventricular failure
in the pulmonary system.
V Heart Failure
Clinical findings
Left-sided failure
Subjective: dyspnea from fluid within the lungs;
orthopnea; fatigue and restlessness

Objective: crackles; peripheral cyanosis; frothy,
blood-tinged sputum; dry, non-productive cough
V Heart Failure
Clinical findings
Right-sided failure
Subjective: abdominal pain; fatigue; bloating; nausea
Objective: dependent, pitting edema that often

subsides at night when legs are elevated; ankle
edema is frequently the first sign of HF; ascites;
hepatomegaly; anorexia; respiratory distress;
increased CVP; diminished urinary output.
V Heart Failure
Therapeutic interventions
Rest in Fowlerǯs position to reduce cardiac workload
Morphine SO4 to reduce anxiety and dyspnea
O2 therapy; in acute ventricular failure endotracheal

intubation and a ventilator
Decrease cardiac workload with diuretics, venous
vasodilators, vein and arteriole dilators, ACE

inhibitors and beta-adrenergic antagonists
Increase pump performance with cardiac glycosides,
inotropes
V Heart Failure
K-supplements to prevent digitalis toxicity and
hypokalemia
Na-restricted diet to limit fluid retention and
promote fluid-excretion
A paracentesis if ascites exists and is causing
respiratory distress
V Heart Failure
Nursing care
Assessment:
Baseline vital signs
Body weight; circumference of edematous extremities
Electrolyte levels (sodium, chloride, potassium)
Intake and Output
V Heart Failure
Nursing care
Diagnosis:
Decreased cardiac outpit r/t impaired cardiac
function
Excess fluid volume r/t impaired excretion of sodium
and water
Impaired gas exchange r/t excessive fluid in
interstitial space
V Heart Failure
Planning/Implementation
Maintain the client in HBR
Elevate extremities except when the client is in acute
distress
Frequently monitor VS
Change positions frequently
Monitor intake and output
Restrict fluids as ordered

V Vascular disease: Thrombophlebitis, Varicose
veins and Peripheral Vascular Disease
Etiology and pathophysiology
Thrombus: a clot composed of platelets, fibrin,
clotting factors and cellular debris attached to the
interior wall of an artery or vein
Embolus: a clot or solid particle carried by the
bloodstream, which may interfere with tissue
perfusion in an artery or vein
Arterial disorders involve depriving oxygen to a body
part or tissue.
Reduced blood flow resulting from atherosclerosis,
thrombus or embolus
Buergerǯs disease (thromboangitis obliterans)
Peripheral circulation impaired by inflammatory
occlusions of peripheral arteries
Incidence is highest in young adult males who smoke
Arterial disorders involve depriving oxygen to a body
part or tissue.
Raynaudǯs disease
Spasms of digital arteries thought to be caused by
abnormal response of the SNS to cold or emotional
stress, usually bilateral and primarily occurs in young
females.
Raynaudǯs phenomenon is episodic arterial spasm of
the extremities secondary to another disease or
abnormality
Venous disorders involve a problem with
transportation of blood back to the heart from the
capillary beds as a result of changes in smooth
muscle around vessels.
Thrombophlebitis: inflammation of a vein associated with
clot formation; risk factors include immobilization, venous
stasis, vessel trauma, pregnancy, obesity and pelvic surgery
Venous disorders
Varicose veins occur when veins in lower extremities
become dilated, congested, tortuous as a result of weakness
of valves or loss of elasticity of vessel walls. Risk factors
include family history, prolonged standing, leg trauma,
thrombophlebitis.
Clinical Findings
Peripheral arterial disorders
Subjective: paresthesia; aching to severe or burning
pain
Objective: pallor or cyanosis; gangrenous ulcers and
diminished pulses in Buergerǯs disease
Clinical Findings
Varicose veins
Subjective: heaviness and fatigue in the legs with
cramping that increases at night
Objective: positive venogram; brown skin
discoloration, stasis ulcers
Clinical Findings
Thrombophlebitis
Subjective: pain on dorsiflexion of affected extremity
(Homanǯs sign); may be asymptomatic until embolus
is released and occludes organ.
Objective: swollen limb with hard veins that are
sensitive to pressure; redness and warmth of area
along the vein.
Peripheral vascular disease
Sympathectomy to sever the sympathetic ganglia supplying
the area; there is local vasodilation with improved
circulation
Femoropopliteal bypass grafting
Amputation
Therapeutic interventions:
Varicose veins
Sclerotheraphy involves injection of a chemical irritant to
the vein.
Surgical intervention through the ligation of the vein above
the varicosity and removal of the involved vein.
Postoperative early ambulation is essential to prevent
formation of thrombi.
Thrombophlebitis
Prophylactic antiembolic stockings and exercises to
promote venous return
Warm moist heat to promote vasodilation
Elevation of extremity to reduce edema
Anticoagulants to prevent recurrence of deep vein
involvement
Vasodilators to prevent vascular spasm
Thrombophlebitis
Thrombolytic therapy to dissolve clot
Nursing care:
Assessment:
Risk factors and subjective data
Affected extremity for pulses, color, temperature and
circumference
Mobility of involved extremity
Nursing care:
Diagnosis:
Ineffective tissue perfusion: peripheral r/t venous
stasis
Risk for impaired skin integrity r/t altered
peripheral tissue perfusion
Chronic pain r/t vascular obstruction
Nursing care:
Observe frequently for signs of vascular impairment
(pallor, cyanosis, coolness)
Apply antiembolism stockings before ambulating
and remove and replace as ordered; if
thrombophlebitis is suspected maintain BR and
notify physician
Nursing care:
Instruct the client to avoid tight and constrictive
clothing that can affect peripheral vessels, cigarette
smoking, massaging legs, maintaining one position
for long periods
In arterial disease keep extremities warm; instruct to
wear gloves when exposed to cold

Nursing care:
If undergoing surgery, monitor for hemorrhage,
assess circulatory status of extremity, keep extremity
elevated, allow out of bed as ordered.
Following a vein ligation: elevate the foot of the bed
for the first 24 hours, observe for signs of
hemorrhage, maintain compression dressings, assist
with ambulation.
V Aneurysms
Distention at the site of a weakness in the arterial
wall.
Saccular aneurysm: pouchlike projection on one side
of the artery.
Fusiform aneurysm: entire circumference of the
artery wall is dilated.

Mycotic aneurysm: tiny weaknesses in arterial walls
resulting from infection.
V Aneurysms
Dissecting aneurysm: tear in the inner lining of an
arteriosclerotic aortic wall causes blood to form a
hematoma between layers of the artery compressing
the lumen.
Causes: congenital weakness; trauma;
atherosclerosis(common cause of both thoracic and
abdominal aneurysms)
Surgical emergency if ruptured.
V Aneurysms
Occur most frequently in middle-aged white males
Risk factors: history of hypertension, obesity, stress,
hypercholesterolemia, cigarette smoking, familial

tendency
V Aneurysms
Clinical Findings:
Thoracic aortic aneurysm
Subjective: may be asymptomatic; dyspnea; dysphagia; pain
resulting from pressure against the nerves or vertebrae
Objective: hoarseness, cough and aphonia from
impingement on laryngeal nerve; unequal pulses and
arterial pressure in upper extremities; trachea may be
displaced from midline because of adhesions between
trachea and aneurysm.
V Aneurysms
Clinical Findings:
Abdominal aortic aneurysm
Subjective: may be asymptomatic; lower back or abdominal
pain (severe if aneurysm is leaking); sensory changes in the
lower extremities if aneurysm ruptures.
Objective: hypertension; pulsating abdominal mass;
mottling of the lower extremities if aneurysm ruptures;
increased abdominal girth if aneurysm ruptures.
V Aneurysms
Clinical Findings:
Dissecting aortic aneurysm
Subjective: restlessness; anxiety; severe pain
Objective: diminished pulses; signs of shock
V Aneurysms
Resection of the aneurysm and use of a Teflon or
Dacron graft
If the aorta is involved the surgical procedure would
involve using a cardiopulmonary bypass
Medical treatment is aimed at decreasing cardiac
output and blood pressure through the use of drugs.

V Aneurysms
Nursing care
Assessment: History of risk factors, pulsation in
abdomen, history of pain
Diagnosis:
Ineffective tissue perfusion: peripheral r/t impaired
arterial circulation
Risk for deficient fluid volume: hemorrhage r/t potential
blood loss
V Aneurysms
Nursing care
Perform neurovascular assessment of extremities
Monitor hemodynamic status
Record intake and output, renal failure may occur after
surgery
Administer narcotics as ordered to alleviate pain
Apply abdominal binders to provide support when the
client is coughing, deep breathing and ambulating
Prevent flexion of hip and knees to eliminate pressure on
the arterial wall.
V Shock
Hypovolemic: occurs when there is a loss of fluid
resulting in inadequate tissue perfusion; caused by
excessive bleeding, diarrhea, vomiting, fluid loss
from burns.
Cardiogenic: occurs when pump failure causes
inadequate tissue perfusion; caused by heart failure;

myocardial infarction; cardiac tamponade.
V Shock
Neurogenic: caused by rapid vasodilation and
subsequent pooling of blood in the peripheral blood
vessels; caused by spinal anesthesia; emotional
stress; drugs that inhibit the SNS
Anaphylactic: caused by an allergic reaction that
causes a release of histamine and subsequent

vasodilation.
Septic: reaction to bacterial toxins (gram negative),
which results in the leakage of plasma into tissues

V Shock
Clinical Findings:
Subjective: apprehension; restlessness; paresis of
extremities
Objective: weak, rapid, thready pulse; diaphoresis;
cold; clammy skin; pallor; decreased urine output;
progressive loss of consciousness; decreased mean
arterial pressure.
V Shock
Aimed at correcting the underlying cause
Fluid and blood replacement
O2 therapy, ventilator
Vasoconstricting drugs to increase blood pressure
Cardiac and hemodynamic monitoring
Antihistamines for anaphylactic shock
Cardiotonics for cardiogenic shock
Antibiotics for septic shock

V Shock
Elevation of lower extremities to ensure circulation
to vital organs.
V Shock
Nursing care
Assessment: history of causative and risk factors
from client; fluid intake and output over the previous
24 hours; signs of covert bleeding: weak, thready
pulse; hypotension; increased respirations; cold
clammy skin.
V Shock
Nursing care
Diagnosis:
Ineffective tissue perfusion: cardiopulmonary r/t
arterial/venous blood flow exchange problems

Risk for injury r/t prolonged shock resulting in
multiple organ failure
Deficient fluid volume r/t loss of fluid
V Shock
Nursing care
Planning/Implementation:
Keep the client warm, place in supine position
Monitor hemodynamic status and vital signs
Monitor urine output and specific gravity
Allay clientǯs anxiety
Administer IV fluids as ordered
Monitor O2 sat and provide O2 therapy as indicated.

V Anemias and Blood disorders
Iron deficiency anemia: most common cause is
bleeding r/t GI bleeding, menstruation; other causes
include inadequate dietary intake, malabsorption
and increased demand
Folate deficiency: amount of folic acid absorbed or
ingested is insufficient to synthesize DNA, RNA and

proteins; associated with alcoholism, malabsorption,
pregnancy and lactation
Pernicious anemia: lack of intrinsic factor in the
stomach prevents the absorption of Vit B12 which
reduces the number of erythrocytes formed.
Aplastic anemia: bone marrow is depressed or
destroyed by a chemical or drug leading to
leukopenia, thrombocytopenia, decreased
erythrocytes and decreased leukocytes
(agranulocytosis)
Hemolytic anemia: excessive or premature
destruction of red blood cells. There are many
causes which include sickle cell anemia, thalassemia,,
antibody reactions, infection and toxins.
Polycythemia vera: a sustained increase in the
number of RBC, WBC, and platelets, with an

increased viscosity of the blood
Thrombocytopenia purpura: appears to result from
the production of an antiplatelet antibody that coats
the surface of platelets and facilitates their
production by phagocytic leukocytes.
Clinical Findings:
Subjective: fatigue, headache; paresthesias; dyspnea;
sore mouth with pernicious anemia; gum bleeding
and epistaxis with thrombocytopenic purpura
Objective: ankle edema, dry, pale mucous
membranes, pallor (except polycythemia vera),
decreased Hgb, RBC, ferritin, increased iron-binding
capacity, megaloblastic condition of the blood with
Fe-deficiency anemia, beefy red tongue, lack of
intrinsic factor, positive Romberg test with
pernicious anemia.
Clinical Findings:
Objective: Fever, bleeding from mucous membranes,
decreased WBC, RBC and platelets with aplastic
anemia, increased Hgb, purple-red complexion with
polycythemia vera, low platelet count, ecchymotic
areas, hemorrhagic petechiae with
thrombocytopenic purpura.
Improve diet: include ascorbic acid which stimulates
Fe uptake
Vitamin supplements: iron, Vit B12, folic acid
Blood transfusions (except for polycythemia vera)
Corticosteroids and androgens to stimulate bone
marrow function; bone marrow transplant

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of elevated BP on separate occassions.

Etiology is complex; begins insidiuosly; changes in

on 3 separate occasions; retinal changes; renal

third drug of a different classification is added.

Relaxation modalities such as biofeedback and

V Unstable Angina (Preinfarction Angina, Crescendo Angina,

V Variant Angina (Prinzmetalǯs Angina)

CABG if medical regimen not successful

possibility of heart damage

Reinforce need to avoid nonaerobic exertion and

3 fatty acids, increase intake of high-fiber foods

system feeding into that side.

orthopnea; fatigue and restlessness

Objective: dependent, pitting edema that often

O2 therapy; in acute ventricular failure endotracheal

vasodilators, vein and arteriole dilators, ACE

Change positions frequently

Monitor intake and output

Restrict fluids as ordered

wear gloves when exposed to cold

artery wall is dilated.

hypercholesterolemia, cigarette smoking, familial

output and blood pressure through the use of drugs.

inadequate tissue perfusion; caused by heart failure;

causes a release of histamine and subsequent

which results in the leakage of plasma into tissues

Vasoconstricting drugs to increase blood pressure

Cardiac and hemodynamic monitoring

Antihistamines for anaphylactic shock

Cardiotonics for cardiogenic shock

Antibiotics for septic shock

arterial/venous blood flow exchange problems

Monitor hemodynamic status and vital signs

Monitor urine output and specific gravity

Allay clientǯs anxiety

Administer IV fluids as ordered

Monitor O2 sat and provide O2 therapy as indicated.

ingested is insufficient to synthesize DNA, RNA and

number of RBC, WBC, and platelets, with an

Blood transfusions (except for polycythemia vera)

Corticosteroids and androgens to stimulate bone

marrow function; bone marrow transplant

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