Digiulio M., Keogh J. Medical-Surgical Nursing Demystified
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CHAPTER 1 Cardiovascular System
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Weak or absence of pulse in affected area because blood flow is reduced
or blocked.
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Decreased temperature distal to the blockage because of restricted blood
flow.
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Pallor or patchy coloring (mottling) of affected area because of reduced
tissue oxygenation.
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Dependent rubor (increased redness when legs are lower).
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Hair loss on extremities.
INTERPRETING TEST RESULTS
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Doppler ultrasonography of affected area.
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Arteriography. Dye is injected into the affected artery enabling an outline of
the artery and blockage to be seen in an x-ray.
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Ankle brachial index (ABI) helps to determine the amount of arterial insuf-
ficiency.
TREATMENT
The goal of treatment is to maintain adequate blood flow to the area and avoid tis-
sue damage. Patients are encouraged to maintain activity and reduce risks for dis-
ease, such as smoking, as well as to control blood pressure and monitoring diabetes.
Medical treatment:
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Exercise.
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Smoking cessation.
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Decrease in lipids, depending on what the labwork shows.
Surgical treatment:
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Femoropopliteal bypass graft: A vessel from another part of the body is
removed and grafted to the affected artery, permitting blood to bypass the
blockage.
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Percutaneous transluminal angioplasty: A catheter containing a balloon is
inserted into the affected artery. The balloon is inflated, stretching the artery;
this causes a healing response that breaks up plaque on the artery wall.
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Atherectomy: A catheter containing a grinding tool is inserted into the
affected artery and is used to grind plaque from the artery wall.
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Embolectomy: Surgical removal of a blood clot from the affected artery.
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Thromboendarterectomy: Surgical removal of atherosclerotic tissue from the
affected artery.
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Laser angioplasty: A laser-tipped catheter is inserted into the affected artery
to remove the blockage.
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Stent: A metal mesh tube is inserted into the affected artery to keep the
artery open.
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Amputation: Surgical removal of the affected limb that contains gangrene
caused by low blood flow or complete blockage of blood to the affected limb.
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Administer antiplatelets medication to enhance blood flow to the lower ex-
tremities. This helps to get blood through the vessels and alleviates symptoms.
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penoxifylline
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cilostazol
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aspirin
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clopidogrel
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dipyridamole
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ticlopidine
NURSING DIAGNOSES
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Fear
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Ineffective tissue perfusion
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Risk for injury
NURSING INTERVENTION
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Monitor most distal pulse to assure circulation exists.
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Compare bilateral pulses.
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Monitor temperature, color of affected area indicating tissue perfusion.
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Support hose.
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Check capillary refill.
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Administer anticoagulant (such as heparin, warfarin) as directed.
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Administer pain medication as directed.
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CHAPTER 1 Cardiovascular System
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Don’t elevate leg or apply heat if occlusion affects the femoral or popliteal
arteries.
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Elevation of the lower extremities makes it harder for the blood flow to get
to the tissues.
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Avoid prolonged sitting, which increases the risk of compression to vessels
(impeding blood flow to lower extremities) and increases risk of clot forma-
tion in lower extremities.
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Explain to the patient:
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How to check pulses in the affected area if there is an absence of a pulse.
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Call the physician if the patient experiences numbness, paralysis, or pain.
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Don’t wear tight clothes; avoid tight knee-high hose, which constricts at
the popliteal space; avoid tight waist bands; ensure wide shoe box.
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Change his/her lifestyle to reduce the risk of peripheral arterial occlusive
disease.
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The importance of regular examinations.
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Foot check daily for open wounds, redness.
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Regular visits to podiatrist.
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Regular consults to vascular MD.
Cardiac Tamponade
WHAT WENT WRONG?
A large amount of liquid accumulates in the sack around the heart (pericardium),
creating pressure on the heart that reduces the filling of ventricles with blood. This
results in a low volume of blood being pumped with each contraction. The accu-
mulating pressure within the pericardium may be due to fluid, pus, or blood. The
end result is decreased stroke volume and cardiac output.
The cause of tamponade may be trauma, postoperative, post-MI, uremia, or
cancer. The fluid may develop rapidly or over time, depending on cause. Tamponade
is a life-threatening condition. The seriousness is related to the amount of pressure
within the heart and the resulting decrease in ventricular filling.
PROGNOSIS
Cardiac tamponade is a medical emergency requiring immediate intervention, such
as drainage of the fluids. Stabilization occurs quickly once the fluid is removed and
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Medical-Surgical Nursing Demystified
pressure is alleviated. If fluid recurs, surgery may be necessary. The prognosis depends
on the etiology of the tamponade.
HALLMARK SIGNS AND SYMPTOMS
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Neck vein distention—accumulation of fluid within the pericardium causes
pressure on the heart, which prevents the venous return from the jugular
veins. This causes distention, more pronounced on inspiration.
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Restlessness due to decreased oxygen to the brain.
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Muffled (dull) heart sounds on auscultation because it’s harder to hear through
fluid.
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Pulsus paradoxus—decrease of 10 mmHg or more in SBP during inspira-
tion—change in pressure within the chest during inspiration, resulting in
decreased ventricular filling, decreased output, fall in SBP.
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Sweating (diaphoresis).
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Difficulty breathing (dyspnea).
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Tachycardia.
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Hypotension.
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Fatigue.
INTERPRETING TEST RESULTS
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Echocardiograph: Ultrasound image of the heart to assess the heart’s posi-
tion, structure, and motion. Ventricle and atria are compressed. Fluid found
within pericardial sac.
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Cardiac catheterization.
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Chest x-ray shows an enlarged heart if large effusion present.
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Electrocardiogram used to rule out other cardiac problems.
TREATMENT
Treatment is directed at reducing the pressure on the heart from the accumulating
fluids in the pericardial sac. The following may be necessary to support and stabi-
lize the patient.
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CHAPTER 1 Cardiovascular System
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Pericardiocentesis: A needle is inserted into the pericardium and fluid is aspi-
rated or drained.
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Administer adrenergic agent—increases heart rate and blood pressure.
NURSING DIAGNOSES
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Anxiety
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Ineffective tissue perfusion
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Decreased cardiac output
NURSING INTERVENTION
•
Monitor vital signs.
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Assure adequate oxygenation.
Cardiogenic Shock
WHAT WENT WRONG?
A drop in blood pressure and blood flow caused by the heart’s inability to pump
blood as a result of a cardiac emergency, such as cardiac tamponade, myocardial
ischemia, myocarditis, or cardiomyopathy (a disease of the heart that deteriorates
the heart muscle). Blood pools in the left ventricle, which causes a back up of blood
into the lungs, resulting in pulmonary edema. Contractions increase to compensate
for the decreased cardiac output, causing an increase in demand for oxygen by
the heart. However, the lungs are not oxygenating the blood sufficiently due to
decreased blood flow; and therefore heart muscles are starved for oxygen.
PROGNOSIS
Treatment needs to find a balance between improving cardiac output and reducing
oxygen needs and cardiac workload of the myocardium. This balance must be
achieved while maintaining perfusion of the heart muscle. Prognosis depends on
finding and treating the underlying cause. Cardiogenic shock requires immediate
treatment, often before the cause is known.
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HALLMARK SIGNS AND SYMPTOMS
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Hypotension, because blood flow decreases below normal.
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Tachycardia, because the heart is trying to pump faster to maintain adequate
blood flow to the body, or occasionally bradycardia, where the heart rate is
less than 60 beats per minute due to myocardial damage.
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Arrhythmias—when the heart muscle does not have enough oxygen it
becomes irritable, making arrhythmias more likely.
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Clammy skin, because oxygenation to tissues is reduced.
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Drop in skin temperature because of reduced circulation as a result of
hypotension.
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Urine output less than 30 ml per hour (oliguria) because the kidneys are not
being perfused.
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Crackles heard in the lungs secondary to pulmonary edema, meaning fluidis
building up in lungs.
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Confusion due to poor perfusion.
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Distended jugular veins—sign of fluid overload, inability of heart to manage
fluid coming into heart.
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Cyanosis of lips, peripheral extremities due to poor perfusion.
INTERPRETING TEST RESULTS
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Chemistry—check electrolytes, kidney function to ascertain kidney perfusion;
calcium level is increased or decreased secondary to muscle contractility.
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Echocardiogram—to look for ventricular rupture, pericarditis, or valve dys-
function.
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Electrocardiogram:
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Q-wave enlarged due to heart failure.
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Elevation of ST-waves is a sign of ischemia.
TREATMENT
Treatment is based on medical support for the heart until etiology (cause) can be
determined. In cardiogenic stroke, the stroke volume and the heart rate must be in-
creased to keep the organs perfused. The effects of the following medications should
accomplish this.
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CHAPTER 1 Cardiovascular System
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Administer vasodilator—dilates blood vessels (arterial and venous) to decrease
the venous return to the heart and reduces the peripheral arterial resistance
(what the heart has to pump against).
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Nitroprusside; nitroglycerin.
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Administer adrenergic agent—to increase the heart rate and blood pressure:
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epinephrine.
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Administer inotropes strengthens the heart beat, improves contractions, pro-
duces peripheral vasoconstriction:
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dopamine
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dobutamine
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inammone
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milrinone
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Administer vasopressor decreases blood flow to all organs except the heart
and brain:
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norepinephrine
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Provide supplemental oxygen—may need to be via intubation.
NURSING DIAGNOSES
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Ineffective tissue perfusion
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Decreased cardiac output
NURSING INTERVENTION
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Monitor vital signs—look for changes in BP, P, R.
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Monitor heart sounds.
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Monitor Swanz Ganz catheter is a catheter placed into the pulmonary artery
to check for pressures in the heart, vessels, and lungs.
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Test capillary refill.
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Monitor arterial blood gas to learn pH, acidosis or alkalosis, bicarb level.
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Monitor respiratory status—due to poor perfusion, these patients are in res-
piratory distress; mechanical ventilation may be needed.
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Place the patient on bed rest.
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Medical-Surgical Nursing Demystified
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Monitor intake and output of fluids—look for adequate renal perfusion.
Without sufficient cardiac function, the patient will not have enough blood
flow to the kidneys to get adequate filtration.
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Explain to the patient:
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Which symptoms to be aware of and when to call the doctor.
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Take rest periods.
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Call the physician if there are signs of fluid overload—weight increase,
shortness of breath, fatigue, dependent edema.
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Record weight each day and call the physician, nurse practitioner, or
physician assistant if there is an increase of 3 lbs (1.4 kg).
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Change to a low-sodium, low-fat diet.
Cardiomyopathy
WHAT WENT WRONG?
The middle layer of the heart wall that contains cardiac muscle (myocardium)
weakens and stretches, causing the heart to lose its pumping strength and become
enlarged. The heart remains functional; however, contractions are weak, resulting
in decreased cardiac output. Most are idiopathic and not related to the major causes
of heart disease. The three types of cardiomyopathy are:
1. Dilated cardiomyopathy (common): The heart muscle thins and enlarges,
which leads to congestive heart failure. Progressive hypertrophy and dilata-
tion result in problems with pumping action of ventricles.
2. Hypertrophic cardiomyopathy: The ventricular heart muscle thickens, result-
ing in outflow obstruction or restriction. There is some blood flow present.
3. Restrictive cardiomyopathy (rare): The heart muscle becomes stiff and re-
stricts blood from filling ventricles, usually as a result of amyloidosis, radi-
ation, or myocardial fibrosis after open-heart surgery.
PROGNOSIS
Prognosis is variable. Sudden cardiac death is a possible outcome in dilated or
hypertrophic cardiomyopathy; arrhythmia is often a precursor to sudden death.
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CHAPTER 1 Cardiovascular System
HALLMARK SIGNS AND SYMPTOMS
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Asymptomatic—Many clients with hypertrophic cardiomyopathy (HCM)
are asymptomatic. Those with signs do not present until their mid-twenties.
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Dyspnea—The most frequent symptom is shortness of breath due to increase
pressure in the lungs. The heart may not sufficiently relax resulting in higher
pressure and a backup of blood into the lungs.
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Angina—Clients experience chest pain related to increase oxygen demand
of the extra heart muscle and due to thick, narrowing coronary blood vessels
within the heart’s wall
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Syncope—Fainting is caused by heart arrhythmias related to the inability of
the cardiac muscle to conduct electrical impulses.
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Sudden death—Young adults are at risk of sudden death during physical
exercise resulting from ventricular fibrillation, which is a cardiac arrhythmia.
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Abnormal heart sounds
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Murmur, which is the sound of turbulence results from abnormal blood flow
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S3, which is a third heart sound commonly heard in heart failure. S3 is a
soft sound made by the vibration of the ventricular wall when the ventri-
cle fills too rapidly. S3 is heard after the S2 heart sound and is best found
over the apex of the left ventricle, which is the fourth intercostal space
along the mid-clavicular line
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S4, which is the heart sound heard before the S1 heart sound is the result
of the heart being too stiff. This is vibration of the valves and the ven-
tricular walls when the atria contracts and the ventricles fill.
INTERPRETING TEST RESULTS
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Chest x-ray (CXR) shows enlarged heart, pulmonary congestion.
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Echocardiography shows left ventricular hypertrophy (LVH) and dysfunc-
tion in dilated and hypertrophic cardiomyopathy; small ventricular size and
function in restrictive cardiomyopathy.
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Electrocardiogram: ST changes, conduction abnormalities, LVH.
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Left ventricular hypertrophy shows as a broad QRS wave, usually in leads
4, 5, and 6 because of high voltage.
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Cardiac catheterization—to measure chamber pressures, cardiac output, ven-
tricular function, but is often unable to add to information that has already
been received from echocardiogram.
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Medical-Surgical Nursing Demystified
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Exercise testing may show poor cardiac function not evident in a resting
state.
TREATMENT
Treatment is based on the specific cause. Avoiding the offending drug/treatment is
imperative. Manage the underlying disease and provide cardiac support; however,
few therapies can halt the process of cardiomyopathy.
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Change to a low-sodium diet.
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Beta adrenergic blockers—cause the heart to beat slowly, allowing more
time for ventricular filling and improve contractile function:
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propranolol, nadolol, metoprolol (for hypertropic cardiomyopathy)
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Angiotensin-converting enzyme (ACE) inhibitors—to decrease left ventric-
ular filling pressures.
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Calcium channel blockers—reduced cardiac workload by increasing contrac-
tile ability:
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verapamil (for hypertrophic cardiomyopathy)
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Diuretics reduce fluid retention:
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furosemide, bumetanide, metolazone (for dilated cardiomyopathy)
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spironolactone (aldosterone antagonist)
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Administer inotropic agent to enable the heart to have greater contractile
force:
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dobutamine
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milrinone
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digoxin (for dilated cardiomyopathy)
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Administer oral anticoagulant to reduce the coagulation of blood:
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warfarin (for dilated and hypertrophic cardiomyopathy)
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Implantable cardioverter-defibrillator for high risk.
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Myectomy—incision into septum and removal of tissue.
NURSING DIAGNOSES
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Activity intolerance
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Impaired gas exchange
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Decreased cardiac output