MANAGEMENT OF PATIENTS WITH CORONARY Metabolic syndrome:

VASCULAR DISORDERS •Insulin resistance

•Central obesity
Coronary Artery Disease (CAD) •Dyslipidemia
•Most prevalent type of cardiovascular disease in adults •BP persistently high
•Proinflammatory state
•CAD results from the narrowing of the coronary •High fibrinogen level
arteries over time due to atherosclerosis (coronary
atherosclerosis) Prevention:
•Controlling Cholesterol Abnormalities
•The primary effect of CAD is the loss of oxygen and •Dietary Measures
nutrients to myocardial tissue because of diminished •Promoting of Cessation of Tobacco Use
coronary blood flow. •Managing hypertension
•Controlling diabetes
Coronary Atherosclerosis •Gender
•An abnormal accumulation of lipid, or fatty, substances
and fibrous tissue in the vessel wall. Diagnostic studies:
Electrocardiography
•These substances create blockages or narrow the a. When blood flow is reduced and ischemia occurs, ST-
vessel in a way that reduces blood flow to the segment depression, T-wave inversion, or both is
myocardium. noted; the ST segment returns to normal when the
blood flow returns.
Clinical Manifestation
•According to: location and degree of narrowing of the b. With infarction, cell injury results in ST segment
arterial lumen, thrombus formation, and obstruction of elevation, followed by T wave inversion and an
blood flow to the myocardium. abnormal Q wave.

•usually progressive, causing an inadequate blood Cardiac Catheterization

supply that deprives the muscle cells of oxygen a. Cardiac catheterization provides the most definitive
needed for their survival. Condition is known as source for diagnosis; shows the presence of
ischemia atherosclerotic lesions.

•A decrease in blood supply from CAD may even cause Blood lipid levels
the heart to stop abruptly, an event that is called a. elevated.
sudden cardiac death. b. Cholesterol-lowering medications

•Angina pectoris refers to chest pain that is brought Interventions

about by myocardial ischemia. 1. Instruct the client regarding the purpose of diagnostic
medical and surgical procedures and pre-procedure and
Findings during symptomatic periods: post-procedure expectations.
 Chest pain
 Palpitations 2. Assist the client to identify risk factors that can be
 Dyspnea modified.
 Syncope (fainting bes)
 Cough or hemoptysis 3. Assist the client to set goals to promote lifestyle
 Excessive fatigue changes to reduce the impact of risk factors.

Risk Factors 4. Assist the client to identify barriers to compliance

Nonmodifiable Risk Factors with the therapeutic plan and to identify methods to
•Family history of coronary heart disease overcome barriers.
•Increasing age
•Gender 5. Instruct the client regarding a low-calorie, low
•Race (higher incidence of heart disease in African sodium, low-cholesterol, and low-fat diet, with an
Americans than in Caucasians) increase in dietary fiber.

Modifiable Risk Factors 6. Stress to the client that dietary changes are not
•High blood cholesterol level temporary and must be maintained for life; instruct the
•Cigarette smoking, tobacco use client regarding prescribed medications.
•Hypertension
•Diabetes mellitus 7. Provide community resources to the client regarding
•Lack of estrogen in women exercise, smoking cessation, and stress reduction as
•Physical inactivity appropriate.
•Obesity
Medications
1. Nitrates to dilate the coronary arteries and decrease
preload and afterload
2. Calcium channel blockers to dilate coronary arteries
and reduce vasospasm
3. Cholesterol-lowering medications to reduce the
development of atherosclerotic plaques
4. b-Blockers to reduce the BP in individuals who are
hypertensive
Surgical procedures
1. PTCA (Percutaneous Transluminal Coronary
Angioplasty)
2. Laser angioplasty (angioplasty yung bubuksan yung
baradong arteries)
3. Atherectomy (pagtanggal ng plaques sa arteries)
4. Vascular stent (parang catheter)
5. Coronary artery bypass grafting (parang gumagawa
ng “bypass” road for blood kasi barado yung arteries)
Angina Pectoris (pain in the chest)
•Involves episodes of acute chest pain as a result of an
inadequate Oxygen supply to the myocardium due to a
decrease in blood flow from the coronary arteries
•Episodes or paroxysms of pain or pressure in the
anterior chest.
Pathophysiology
a. Angina is usually caused by atherosclerotic disease.
b. Normally, the myocardium extracts a large amount of
oxygen from the coronary circulation to meet its
continuous demands.
c. When the demand increases, flow through the
coronary arteries needs to be increased .
d. When there is a blockage in the coronary artery, flow
cannot be increased and ischemia will result.
Several factors associated with anginal pain are:
•Physical exertion
•Exposure to cold
•Eating a heavy meal
•Stress or any emotion-provoking situation
Types of Angina
Stable Angina - predictable and consistent pain that
occurs on exertion and is relieved by rest. (consistent,
rest)
Unstable Angina (also called preinfarction angina or
crescendo angina) - symptoms occur more frequently
and last longer than stable angina.
•The threshold for pain is lower, and pain may occur at
rest. (frequent, longer, no rest)
Variant Angina (also called Prinzmetal’sangina): -pain
at rest with reversible ST-segment elevation; thought to
be caused by coronary artery vasospasm (no rest,
reversible ST elevation, muscle constriction then
babalik sa heart yung blood)
Intractable or Refractory Angina - severe incapacitating
chest pain (severe, incapacitating)
Silent Ischemia - objective evidence of ischemia (such
as electrocardiographic changes with a stress test), but
patient reports no symptoms. (ischemia, silent
symptoms)
Clinical Manifestations:
•Retrosternal (behind ng sternum)
•Mild to moderate pressure, deep sensation; varied
pattern of attacks: “tightness,” “squeezing,” “crushing”
sensations
•Poorly localized and may radiate
•Feels tightness or a heavy choking or strangling
sensation that has a viselike, insistent quality.
•Weakness or numbness in the arms, wrists, and hands
as well as shortness of breath, pallor, diaphoresis,
dizziness or light headedness, and nausea and vomiting,
may accompany the pain.(Stable or Unstable)
HOY! Mga may DM possibly hindi nakakaramdam ng
angina:
*The patient with diabetes may not have severe pain
with angina because of diabetic neuropathy can blunt
nocireceptor transmission, dulling the perception of
pain.
Assessment and Diagnostic Findings:
•History
•12-lead ECG
•Cardiac biomarker testing
•Serum lipid and enzyme values
•Treadmill stress test/pharmacologic stress test
•Echocardiogram
•Nuclear scan
•Invasive procedure: cardiac catheterization/coronary
angiography
Medical management
Decrease the oxygen demand of the myocardium
Increase the oxygen supply
Pharmacologic Therapy
Nitroglycerin (NTG)
•Nitrates are the standard treatment for angina
pectoris.
•Potent vasodilator that improves blood flow to the
heart muscle and relieves pain.
•Dilates primarily the veins, to a lesser extent, the
arteries.
•Nitrates also relax the systemic arteriolar bed,
lowering blood pressure and decreasing afterload.
NTG might be given in several routes:
•Sublingual or spray
•Oral capsule
•Topical agent, and
•IV
Read! (Mga about sa pag-take ng NTG)
1. Instruct the patient to make sure the mouth is moist,
the tongue is still, and saliva is not swallowed until the
nitroglycerin tablet dissolves. If the pain is severe, the
patient can crush the tablet between the teeth to
hasten sublingual absorption.
2. Advise the patient to carry the medication at all
times as a precaution. However, because nitroglycerin is
very unstable, it should be carried securely in its original
container (eg, capped dark glass bottle); tablets should
never be removed and stored in metal or plastic
pillboxes.
3. Explain that nitroglycerin is volatile and is
inactivated by heat, moisture, air, light, and time.
Instruct the patient to renew the nitroglycerin supply
every 6 months.
4. Inform the patient that the medication should be
taken in anticipation of any activity that may produce
pain. Because nitroglycerin increases tolerance for
exercise and stress when taken prophylactically (ie,
before angina-producing activity, such as exercise, stair-
climbing, or sexual intercourse), it is best taken before
pain develops.
5. Recommend that the patient note how long it takes
for the nitroglycerin to relieve the discomfort. Advise
the patient that if pain persists after taking three
sublingual tablets
at 5-minute intervals, emergency medical services
should be called.
6. Discuss possible side effects of nitroglycerin,
including flushing, throbbing headache, hypotension,
and tachycardia.
Take note!
Most physicians prescribe application of topical
nitroglycerin paste three or four times daily or every 6
hours (excluding the midnight dose), and application of
the nitroglycerin patch every morning and removed at
10 PM.
*This dosing regimen allows for a 6- to 8-hour
nitrate-free period to prevent the body’s development
of tolerance.
Beta Adrenergic Blocking Agents
•reduce myocardial oxygen consumption by blocking
the beta-adrenergic sympathetic stimulation to the
heart
•The result is a reduction in heart rate, slowed
conduction of an impulse through the heart, decreased
blood pressure, and reduced myocardial contractility
that establishes a more favorable balance between
myocardial oxygen needs and the amount of oxygen
available.
•propranolol (Inderal), metoprolol (Lopressor, Toprol),
and atenolol (Tenormin)
Calcium Channel Blocking Agents
•calcium ion antagonists
•Relax the blood vessels, causing a decrease in blood
pressure and an increase in coronary artery perfusion.
•Myocardial oxygen supply by dilating the smooth
muscle wall of the coronary arterioles
Aspirin
•Prevents platelet activation
•160mg to 325mg dose of aspirin should be given to the
patient with angina as soon as the diagnosis is made
*gastrointestinal upset and bleeding
Heparin
•Unfractionated heparin prevents the formation of
new blood clots. Use of heparin alone in treating
patients with unstable angina reduces the occurrence of
MI.
Heparin bleeding precautions!!!!!!!
•Pressure on bleeding site
•Avoiding IM injections
•Avoiding tissue injury and bruising from trauma or
use of constrictive devices (continuous use of an
automatic BP cuff)
Oxygen Administration
•initiated at the onset of chest pain
•increase the amount of oxygen delivered to the
myocardium and to decrease pain.
•Oxygen inhaled directly increases the amount of
oxygen in the blood.
•The therapeutic effectiveness of oxygen is determined
by observing the rate and rhythm of respirations.
•Pulse oximetry - >95%
Interventions
Immediate management
a. Assess pain; institute pain relief measures.
b. Administer oxygen at 3 L/min by nasal cannula as
prescribed.
c. Assess vital signs and provide continuous cardiac
monitoring and nitroglycerin as prescribed to dilate the
coronary arteries, reduce the oxygen requirements of
the myocardium, and relieve the chest pain.
d. Ensure bed rest is maintained, place the client in
semi-Fowler’s position, and stay with the client.
e. Obtain a 12-lead ECG.
f. Establish an IV access route.
ACUTE CORONARY SYNDROME (ACS) - is an emergent
situation characterized by an acute onset of myocardial
ischemia that results in myocardial death if definitive
interventions do not occur promptly.
The spectrum of ACS includes: Begin routine medical interventions:
•Unstable angina
•NSTEMI MONA
•STEMI •Supplemental oxygen
•Nitroglycerine
Myocardial infarction (MI) - Occurs when myocardial •Morphine
tissue is abruptly and severely deprived of oxygen •Aspirin 162-325 mg
Ischemia can lead to necrosis of myocardial tissue if •Beta blocker
blood flow is not restored. •ACE inhibitor
•Anticoagulation therapy
•Infarction does not occur instantly but evolves over
several hours. Invasive Coronary Artery Procedures

•Physical changes do not occur in the heart until 6
hours after the infarction, when the infarcted area
appears blue and swollen.
*After 48 hours, the infarct turns gray, with yellow
streaks developing as neutrophils invade the tissue. By 8
to 10 days after infarction, granulation tissue forms.
Over 2 to 3 months, the necrotic area develops into a
scar; scar tissue permanently changes the size and
shape of the entire left ventricle.
Pathophysiology
•As the cells are deprived of oxygen, ischemia develops,
cellular injury occurs, and over time, the lack of oxygen
results in infarction, or the death of cells.
Assessment
1. Pain (Levine Sign)
2. Nausea and vomiting
3. Diaphoresis
4. Dyspnea
5. Dysrhythmias
6. Feelings of fear and anxiety
7. Pallor, cyanosis, coolness of extremities
Percutaneous Coronary Interventions (PCIs)
•Methods to reperfuse ischemic myocardial tissue
when patients are refractory to more conservative
management methods
Which includes:
1. Percutaneous Transluminal Coronary Angioplasty
(PTCA),
2. Intracoronary stent implantation
Percutaneous Transluminal Coronary Angioplasty
(PTCA)
•The purpose of PTCA is to improve blood flow within a
coronary artery by “cracking” the atheroma.
•This invasive interventional procedure is carried out in
the cardiac catheterization laboratory. The coronary
arteries are examined by angiography
Coronary Artery Stent
•After PTCA, a portion of the plaque that was not
removed may block the artery. The coronary artery may
recoil (constrict) and the tissue remodels, increasing the
risk for restenosis.

Risk factors •A coronary artery stent is placed to overcome these

1. Atherosclerosis risks.
2. Coronary artery disease
3. Elevated cholesterol levels •A stent is a woven mesh that provides structural
4. Smoking support to a vessel at risk of acute closure. The stent is
5. Hypertension placed over the angioplasty balloon.
6. Obesity
7. Physical inactivity SURGICAL PROCEDURES: Coronary Artery
8. Impaired glucose tolerance Revascularization
9. Stress
Coronary Artery Bypass Graft (CABG) - surgical
Diagnostic studies procedure in which a blood vessel from another part of
•Cardiac biomarkers the body is grafted to the occluded coronary artery so
•ECG that blood can flow beyond the occlusion; it is also
•Echocardiography called a bypass graft.
•Cardiac Stress testing
•Cardiac catheterization Candidates for CABG
•Angina that cannot be controlled by medical therapies
Treatment guidelines for AMI •Unstable angina
•Use rapid transit to the hospital. •A left main coronary artery lesion or blockage of more
•Obtain 12-lead ECG to be read within 10 minutes. than 60%
•Obtain laboratory blood specimens of cardiac •Blockage of two or three coronary arteries
biomarkers, including troponin.
•Obtain other diagnostics to clarify the diagnosis
For a patient to be considered for CABG.... Diagnostics
•the coronary arteries to be bypassed must have at • Auscultation: reveals clicking sound; murmur
least a 70% occlusion (60% if it is the left main coronary when left ventricle contracts
artery). • Echocardiography
• Electrocardiography (ECG): may reveal atrial or
•If the lesion involves less than 70% of the artery, ventricular arrhythmia
enough blood can flow through the blocked artery to • Holter monitor for 24 hours: may show
prevent adequate blood flow through the bypass graft. arrhythmia

•As a result, the graft would clot, effectively negating Treatments

the surgery. • Decreased caffeine, alcohol, tobacco, stimulant
intake: decreases palpitations
-------------------------------------------------------------------------- • Fluid intake: maintains hydration
-------------------------------------------------------------------------- • Beta-blocker
VALVULAR HEART DISORDERS • Anticoagulants: prevent thrombus formation
•Valvular heart disease can affect any of the valves in • Antiarrhythmics: prevent arrhythmias
the heart.
Complications
•Diseased valves may have an altered structure, which • Arrhythmias
changes the blood flow. • Infective endocarditis
• Mitral insufficiency from chordal rupture
•Disorders of the endocardium, the innermost lining of
the heart and valves, damage heart valves. MITRAL INSUFFICIENCY/ REGURGITATION - The mitral
valve does not close properly during ventricular systole,
Valvular heart diseases include: causing backward flow of blood during systole.
• Mitral stenosis.
• Mitral regurgitation. • This backward flow can cause heart failure
• Mitral valve prolapse.
• Aortic stenosis. Causes
• Aortic regurgitation • Infective endocarditis or rheumatic heart
disease
• Coronary artery disease
MITRAL VALVE PROLAPSE - The valve cusps bulge into • Aging: over time, degenerative changes can
the left atrium when the left ventricle contracts, weaken the valve
allowing leakage of blood into the atrium
Assessment
Causes • Fatigue; weakness
• Connective tissue disorders : the chordae tendineae • Pansystolic murmur
can become elongated, which allows the mitral valve • If S1 and S2 are audible, the murmur will be
leaflets to open backward into the atrium during heard between these two sounds: lub,
systole. “whoosh,” dub
• Angina: decreased coronary artery circulation
Remember: backflow equals heart failure • Palpitations
• Congenital heart disease • Late signs include signs and symptoms of left-
• Acquired heart disease-CAD sided heart failure
• Rheumatic heart disease: causes valve bulge • nocturnal dyspnea;
due to inflammation • S3;
• pink, frothy sputum; cough; crackles;
Assessment orthopnea; tachycardia; restlessness
Extra heart sound:
• MITRAL CLICK (Mid-to-late systolic click) Diagnostics
• Systolic click is an early sign that a valve leaflet • Auscultation: presence of heart murmur
is ballooning into the left atrium • Electrocardiography
• Late systolic murmur: blood backing up into left • Chest x-ray
atrium • Echocardiography
*Palpitations
Treatment
Assessment if MR exists • Anticoagulants: prevent clots
• Fatigue; weakness: during ventricular systole, • ACE inhibitors: treat mild heart failure
blood backs up into left atrium. • Valvuloplasty: repairs the faulty valve
• Angina: decreased coronary artery circulation • Valve replacement: with a prosthetic valve
• Migraine headaches
• Dizziness
• Orthostatic hypotension
Complications • Prosthetic valve: replaces damaged valve that
• Severe pulmonary edema can’t be repaired
• Embolitic stroke
• Heart failure Complications
• Infection, especially with valve replacement • Embolitic stroke
surgery • Heart failure
• Pulmonary embolism • Infection, especially with valve replacement
surgery
MITRAL STENOSIS - is narrowing of the mitral valve. The • Pulmonary embolism
left atrium meets resistance as it attempts to move
blood forward into left ventricle. AORTIC STENOSIS - Narrowing of the aortic valve
opening that increases resistance to blood flow from
• Eventually the left atrium dilates and contractility the left ventricle to the aorta.
decreases. Forward flow is decreased and fluid backs
up into lungs. Increased volume in the lungs increases • The left ventricle hypertrophies and weakens, leading
pressure in lungs. to left- sided heart failure

• Remember: more volume, more pressure. Causes

• Age: degenerative changes causing scarring and
• Pulmonary hypertension in turn can lead to right- calcium accumulation in the valve cusps
sided heart failure • Rheumatic fever: causes inflammation of the
cusps that leads to scarring; usually
Causes accompanied by mitral stenosis and leakage
• Acute rheumatic fever or infective endocarditis • Birth defect: valve with two cusps instead of
• Congenital abnormality usual three; valve with abnormal funnel shape;
• Myxoma • calcium accumulates, causing the valve to
• Blood clot reduces blood flow through the become stiff and narrow
mitral valve • Atherosclerosis: lipids can increase calcium
accumulation of the valves
Signs and symptoms
• Exertional dyspnea: the narrowed mitral valve Signs and Symptoms
decreases • Exertional dyspnea: decreased blood supply to
• Orthopnea: fluid accumulates in the lungs and the enlarged heart leads to decreased CO
the client sits up to breathe better • Angina: decreased blood supply to the enlarged
• Nocturnal dyspnea heart is inadequate
• Atrial fibrillation: the enlarged left atrium • Syncope
interferes with normal conduction pathways. • Pulmonary congestion: left-sided heart failure
• Diastolic murmur: turbulent flow occurs at the • Harsh, rasping, crescendo-decrescendo systolic
narrowed valve murmur:
• Murmur is heard after S2. You will hear: • forced blood flow across stenotic valve
lub (S1) dub (S2), whoosh . . . lub dub, whoosh
• JVD, hepatomegaly, peripheral edema, weight Diagnostics
gain, ascites, epigastric discomfort, tachycardia, • Chest x-ray
crackles, pulmonary edema • Echocardiography
• Cardiac catheterization: increased pressure
Diagnostic test across aortic valve; increased left ventricular
• Echocardiography pressures; presence of coronary artery disease
• Electrocardiography
• Chest x-ray Treatments
• Cardiac catheterization • Low-sodium, low-fat, low-cholesterol diet
• Diuretics
Treatment • Cardiac glycosides: control atrial fibrillation
• Prevention of rheumatic fever • Percutaneous balloon aortic valvuloplasty:
• Digoxin, reduces degree of stenosis
• diuretics, • Aortic valve replacement: replaces diseased
• vasodilators, valve
• ACE inhibitors: treat left-sided heart failure
• Oxygen: increases oxygenation AORTIC INSUFFICIENCY/ REGURGITATION - Leakage of
• Anticoagulants: the aortic valve.
• Nitrates: relieve angina
• Beta-adrenergic blockers or digoxin • Each time the left ventricle relaxes, blood leaks back
• Cardioversion into it. (Atria are contracting while ventricles are
• Balloon valvuloplasty: enlarges orifice of relaxing)
stenotic mitral valve
Causes
• Bacterial endocarditis, rheumatic fever
• Connective tissue diseases: direct damage of
the heart valves can occur, causing valvular
regurgitation or valvular stenosis
Signs and Symptoms
• Left-sided heart failure such as nocturnal
dyspnea, S3, pink fothy sputum, cough,
crackles, orthopnea, tachycardia, restlessness
• Diastolic murmur: blood is backing up into left
ventricle from aorta during diastole.
• You will hear S1, S2, then the murmur: “lub,
dub, whoosh”
Tests
• Chest x-ray
• Echocardiography
• Electrocardiography
• Cardiac catheterization: shows coronary artery
disease
Treatments
• Oxygen: increases oxygenation
• Vasodilators: reduce systolic load and
regurgitant volume
• Valve replacement with prosthetic valve:
removes diseased aortic valve
• Low-sodium diet
• Diuretics
• Nitroglycerin: relieves angina
• most common valvuloplasty procedure is
commissurotomy.
Commissure
• Each valve has leaflets; the site where the
leaflets meet
• The leaflets may adhere to one another and
close the commissure
• Less commonly, the leaflets fuse in such a way
that, in addition to stenosis, the leaflets are
also prevented from closing completely,
resulting in a backward flow of blood.
• splitting or separating fused cardiac valve
leaflets
CLOSED COMMISSUROTOMY/BALLOON
VALVULOPLASTY
Mitral valvuloplasty is contraindicated for patients with:
• Left atrial or ventricular thrombus, severe aortic
root dilation, significant mitral valve
regurgitation
OPEN COMMISSUROTOMY
• Open commissurotomies are performed with
direct visualization of the valve.
• general anesthesia
• median sternotomy or left thoracic incision is
made.
• Cardiopulmonary bypass is initiated, and an
incision is made into the heart.
• A finger, scalpel, balloon, or dilator may be used
to open the commissures.

Complications ANNULOPLASTY
• Left-sided heart failure • Annuloplasty is the repair of the valve annulus
• Pulmonary edema (junction of the valve leaflets and the muscular
• Myocardial ischemia heart wall).
• General anesthesia and cardiopulmonary
bypass are required for all annuloplasties.
• The procedure narrows the diameter of the
valve’s orifice and is useful for the treatment of
valvular regurgitation

• To annuloplasty techniques:
1. annuloplasty ring
SURGICAL MANAGEMENT: VALVE REPAIR AND 2. tacking the valve leaflets
REPLACEMENT PROCEDURES
Valvuloplasty: repair of a stenosed or regurgitant LEAFLET REPAIR
cardiac valve • Leaflet repair for elongated, ballooning, or
Repair may be made to the: other excess tissue leaflets is removal of the
• commissures (between the leaflets)-- extra tissue.
commissurotomy, • The elongated tissue may be folded over onto
• annulus of the valves---- annuloplasty itself (tucked) and sutured (leaflet plication). A
• leaflets or to the chordae---- chordoplasty wedge of tissue may be cut from the middle of
the leaflet and the gap sutured closed (leaflet
Valvuloplasty resection).
• Require general anesthesia
• Often require cardiac catheterization laboratory CHORDOPLASTY
• Chordoplasty is the repair of the chordae
-otomy means tendineae.
cutting into a part of the body or to make an incision or • The mitral valve is involved with chordoplasty
cut into (because it has the chordae tendineae); seldom
is chordoplasty required for the tricuspid valve.

Commissurotomy VALVE REPLACEMENT

 • Prosthetic valve replacement began in the
1960s.
• When valvuloplasty or valve repair is not a
viable alternative, such as when the annulus or
leaflets of the valve are immobilized by
calcifications, valve replacement is performed.
• MECHANICAL VALVES
• The mechanical valves are of the ball-and-cage
or disk design.
• Mechanical valves are used if the patient has
renal failure, hypercalcemia, endocarditis, or
sepsis and requires valve replacement.
• The mechanical valves do not deteriorate or
become infected as easily as the tissue valves
used for patients with these conditions.
• Thromboemboli are significant complications
• anticoagulation with warfarin is required.
VALVE REPLACEMENT
• TISSUE OR BIOLOGIC VALVES
• Tissue valves are of three types:
(1) xenografts, (2) homografts, and (3)
autografts.
• Tissue valves are less likely to generate
thromboemboli, and long-term anticoagulation
is not required.
• Tissue valves are not as durable as mechanical
valves and require replacement more
frequently.
BIOPROSTHESES: XENOGRAFTS OR HETEROGRAFTS
• most are from pigs (porcine) and from cows
(bovine
• Viability is 7 to 10 years.
• They do not generate thrombi, thereby
eliminating the need for longterm
anticoagulation.
BIOPROSTHESES: HOMOGRAFTS, OR ALLOGRAFTS
• human valves are obtained from cadaver tissue
donations
• harvested and stored cryogenically.
• last for about 10 to 15 years
• Not thrombogenic and are resistant to subacute
bacterial endocarditis.
• They are used for aortic and pulmonic valve
replacement
BIOPROSTHESES: AUTOGRAFTS
• Autografts (autologous valves) are obtained by
excising the patient’s own pulmonic valve and a
portion of the pulmonary artery for use as the
aortic valve.
• Anticoagulation is unnecessary because the
valve is the patient’s own tissue and is not
thrombogenic.
CARDIOMYOPATHIES
• Cardiomyopathy is a heart muscle disease
associated with cardiac dysfunction.
• It is classified according to the structural and
functional abnormalities of the heart muscle
•
There are three types of cardiomyopathy:
• Restrictive: ventricles are stiff and cannot fill properly.
• Hypertrophic: walls of the ventricles thicken and
become stiff.
• Dilated: ventricles enlarge but are not able to pump
enough blood for the body’s needs.
Ischemic cardiomyopathy is a term frequently used to
describe an enlarged heart caused by coronary artery
disease, which is usually accompanied by heart failure
DILATED CARDIOMYOPATHY (DCMP)
• most common form of cardiomyopathy
• formerly named congestive cardiomyopathy,
but DCM may exist without signs and
symptoms of congestion.
• Microscopic examination of the muscle tissue
shows diminished contractile elements of the
muscle fibers and diffuse necrosis of
myocardial cells. The result is poor systolic
function.
• Embolic events caused by ventricular and atrial
thrombi as a result of the poor blood flow
through the ventricle may also occur.
Causes
• Chemotherapy
• Alcohol and drugs
• Coronary heart disease
• Viral or bacterial infections
• Pregnancy-induced
Signs and Symptoms
• Shortness of breath and orthopnea,
• Left-sided heart failure
• Right-sided heart failure
• Peripheral cyanosis, tachycardia Low cardiac
output
• Murmur Leaking heart valves
• Arrhythmia: Stretching of the heart muscle
leads tocabnormal heart rhythms
• Chest pain; palpitations Arrhythmias may be felt
as pain or palpitations
• Syncope Decreased cardiac output
HYPERTROPHIC CARDIOMYOPATHY (HCM)
• Heart muscle increases in size and mass,
especially along the septum
• The increased thickness of the heart muscle
reduces the size of the ventricular cavities and
causes the ventricles to take a longer time to
relax, making it more difficult for the ventricles
to fill with blood during the first part of diastole
and making them more dependent on atrial
contraction for filling.
OBSTRUCTIVE OR NON OBSTRUCTIVE
HYPERTROPHIC CARDIOMYOPATHY (HCM) • Removal of blood at regular intervals: reduces
• Uncontrolled hypertension amount of stored iron in clients with iron
• Inherited gene overload.
• Acromegaly: Excessive growth of the heart • Heart transplant.
muscle due to overproduction of growth
hormone INFECTIOUS DISEASES OF THE HEART
• Among the most common infections of the
Signs and symptoms heart are infective endocarditis, myocarditis,
• Fatigue; weakness and pericarditis.
• Late signs include signs and symptoms of left- • The ideal management is prevention.
sided heart failure
• Arrhythmias RHEUMATIC ENDOCARDITIS
• Chest pain • Acute rheumatic fever-- school-age children
• Palpitations • group A beta-hemolytic streptococcal
• Faintness; dizziness pharyngitis (strep throat)
• Sudden cardiac death:Lethal arrhythmias • Treatment: antibiotics
leading to death • The Streptococcus is spread by direct contact
with oral or respiratory secretions.
Surgical management
• Left ventricular outflow tract surgery RECOGNIZING AND PREVENTING RHEUMATIC FEVER
• Heart Transplantation • Rheumatic fever is a preventable disease.
• Mechanical assist device and Total heart • Eradicating rheumatic fever would eliminate
transplant rheumatic heart disease.
• Penicillin therapy: can prevent almost all
RESTRICTIVE CARDIOMYOPATHY primary attacks of rheumatic fever.
• Restrictive cardiomyopathy (RCM) is • throat culture is the only method by which an
characterized by diastolic dysfunction caused accurate diagnosis of strep throat can be
by rigid ventricular walls that impair ventricular determined
stretch and diastolic filling
The signs and symptoms of streptococcal pharyngitis
• Diseases that change the composition of the are the following:
heart muscle, making it stiff and noncompliant. • Fever
• Chills
• Amyloidosis is a condition where glycoproteins • Sore throat (sudden in onset)
are deposited within the myocardium • Diffuse redness of throat with exudate on
oropharynx
• Accumulation of these glycoproteins in the • Enlarged and tender lymph nodes
heart alters heart function. • Acute sinusitis and acute otitis media (if due to
streptococci
• The heart becomes stiff and rigid, resulting in a
decreased volume in the ventricles and INFECTIVE ENDOCARDITIS
ultimately a decrease in CO • Infective endocarditis is an infection of the
endocardium, heart valves, or cardiac
Signs and symptoms prosthesis
• Signs and symptoms of heart failure:
bradycardia, neck vein distension, peripheral Origin
edema, liver congestion, abdominal ascites • Bacteria: When they attack the heart, they
• Fatigue; weakness attack the valves. *“vegetation”
• Late signs include nocturnal dyspnea, S3, pink • Fungi can proliferate on heart valves
frothy sputum, cough, crackles, orthopnea, • Prosthetic valves: Bacteria easily stick to the
tachycardia, restlessness foreign device
• Recent cardiac surgery: Contamination of the
Diagnostics area during surgery
• ECG • Rheumatic heart disease
• Echocardiography • Systemic lupus erythematosus
• Magnetic resonance imaging • Congenital heart defects: Malformed heart
• Cardiac catheterization valves are more susceptible to colonization
• *Biopsy • Valvular dysfunction
• IV drug abuse: IV drug abusers who do not
Treatments: follow aseptic technique can “inject” bacteria
• 70% of patients die within 5 years of symptom into the blood.
development.
• Medications not helpful.
Signs and symptoms Complications
• Fever • Microemboli or septic emboli traveling to other
• Splenomegaly organs
• Petechia • Stroke
• Hematuria • Heart failure
• Cardiac murmurs • Infection
• Vegetation on the valve • Valve stenosis or regurgitation
• Pleuritic pain • Myocardial erosion
• Fatigue; weakness
• Late signs include signs and symptoms of left- MYOCARDITIS
sided Infection and/or clot formation on the • Myocarditis is an inflammatory process
mitral or aortic valves heart failure involving the myocardium.

Prevention • Myocarditis can cause heart dilation, thrombi

• primary prevention in high-risk patients on the heart wall (mural thrombi), infiltration
• Antibiotic prophylaxis: of circulating blood cells around the coronary
• Dental procedures vessels and between the muscle fibers, and
• Tonsillectomy or adenoidectomy degeneration of the muscle fibers themselves.
• Surgical procedures that involve intestinal or
respiratory mucosa Pathophysiology
• Bronchoscopy with a rigid bronchoscope • Myocarditis usually results from a viral,
• Sclerotherapy for esophageal varices bacterial, mycotic, parasitic, protozoal, or
• Esophageal dilation spirochetal infection
• Gallbladder surgery • Myocarditis may result from an allergic reaction
• Cystoscopy to pharmacologic agents
• Urethral dilation
• Urethral catheterization if urinary tract Clinical Manifestations
infection is present • The patient with mild to moderate symptoms
• Urinary tract surgery if urinary tract infection is often complains of:
present • fatigue and dyspnea,
• Prostatic surgery • palpitations, and
• Incision and drainage of infected tissue • occasional discomfort in the chest and upper
• Vaginal hysterectomy abdomen.
• Vaginal delivery
Prevention
Nursing Management • Prevention: appropriate immunizations (eg,
• monitors the patient’s temperature influenza, hepatitis) and
• Heart sounds are assessed • early treatment
• Monitors for signs and symptoms of systemic
embolization Nursing Management
• Assesses for signs and symptoms of organ NURSING ALERT
damage such as stroke (CVA), meningitis, heart  Patients with myocarditis are sensitive to
failure, myocardial infarction, digitalis.
glomerulonephritis, and splenomegaly. • They must be closely monitored for digitalis
• Patient care is directed toward management of toxicity, which is evidenced by dysrhythmia,
infection. anorexia, nausea, vomiting, headache, and
malaise and BLURRED OR DOUBLE VISION and
Diagnostics GREENISH- YELLOW HALOS AROUND IMAGES.
• Blood cultures • Assesses the patient’s temperature
• White blood cell with differential count: • continuous cardiac monitoring with personnel
elevated. and equipment readily available to treat life-
• Complete blood count and anemia panel threatening dysrhythmias.
• Erythrocyte sedimentation rate: elevated. • Elastic compression stockings and passive and
• Creatinine level: elevated. active exercises should be used, because
• Urinalysis: proteinuria, hematuria. embolization from venous thrombosis and
• Echocardiography: shows valvular damage. mural thrombi can occur.
• Electrocardiogram: atrial fibrillation.
PERICARDITIS
Treatments • Pericarditis refers to an inflammation of the
• Antibiotics: given for 2 to 6 weeks IV in high pericardium, the membranous sac enveloping
doses. the heart
• Surgery: repair or replace damaged valve and
remove vegetations.
Pathophysiology
• Infection
• Disorders of connective tissue
• Hypersensitivity states
• Disorders of adjacent structures: myocardial
infarction, dissecting aneurysm, pleural and
pulmonary disease
• Neoplastic disease
• Radiation therapy
• Trauma
• Tuberculosis
• Pericarditis can lead to: pericardial effusion and
cardiac tamponade
Signs and Symptoms
• Pericardial friction rub
• Dysphagia (difficulty swallowing)
• Chest pain: worsens with inspiration and
decreases when the client leans forward; can
radiate to neck, shoulders, chest and arms
Diagnostics
• White blood cell count: elevated.
• Erythrocyte sedimentation rate: elevated.
• Serum creatinine: elevated.
• Pericardial fluid culture: identifies causative
organism in bacterial or fungal pericarditis.
• Blood urea nitrogen: elevated.
• Echocardiography: shows pericardial effusion.
• Electrocardiography: shows elevated ST
segment.
Treatments
• Bed rest as long as fever and pain persist
• NSAIDs: relieves pain and reduces
inflammation.
• Antibacterial, antifungal, antiviral therapy: if
infectious cause.
• Pericardiocentesis: removes excess fluid from
pericardial space.
Nursing Interventions
• RELIEVING PAIN
• patient rest; restrict activity until the pain
subsides
• Because sitting upright and leaning forward is
the posture that tends to relieve pain, chair
rest may be more comfortable.
MONITORING AND MANAGING POTENTIAL
COMPLICATIONS
• Cardiac tamponade.
• Pericardial effusion.
• Infection.
--------------------------------------------------------------------------
--------------------------------------------------------------------------
MANAGEMENT OF PATIENTS WITH COMPLICATIONS
FROM HEART DISEASE
Heart Failure (HF) - often referred to as congestive
heart failure (CHF)
• A clinical syndrome resulting from structural or
functional cardiac disorders that impair the ability of
the ventricles to fill or eject blood.
• is the inability of the heart to pump sufficient blood
to meet the needs of the tissues for oxygen and
nutrients.
CHRONIC HEART FAILURE
Types of HF
• diastolic heart failure
• systolic heart failure
An assessment of the ejection fraction (EF) is performed
to assist in determining the type of HF.
• Heart Failure (HF)
• Low EF is a hallmark of systolic HF
• New York Heart Association (NYHA) classification of
heart failure:
(NYHA) Classification of Heart Failure
Classification of Heart Failure (HF)
• Left-sided heart failure
• Right-sided heart failure
1. Left-sided heart failure - occurs when the left
ventricle fails and cardiac output falls.
• The blood backs up into the left atrium and lungs,
causing pulmonary congestion
2. Right-sided heart failure - also known as cor
pulmonale
• occurs when the right ventricle does not contract
effectively
• This causes blood to back up into the right atrium and
the peripheral circulation, which causes peripheral
edema and engorgement of the kidneys and other
organs
PATHOPHYSIOLOGY
Causes of Left-sided HF
• Coronary artery disease
• Myocardial infarction
• Myocarditis or endocarditis
• Heart valve disorders
• Arrhythmias
• Pulmonary hypertension
• Pulmonary embolism
• Hyperthyroidism
• Hypothyroidism
• Anemia
Clinical manifestations: Left-sided heart failure
• Crackles • Pulmonary edema occurs when capillary fluid leaks
• Dyspnea into the alveoli. Since the alveoli are filled with fluid,
• Nonproductive cough they do not oxygenate the blood very well and the
• Blood tinged, frothy sputum patient will be in respiratory distress.
• Restlessness
• Tachycardia Pathophysiology
• S3 and S4 • Increased hydrostatic pressure that forces fluid out
• Orthopnea of the pulmonary capillaries and to the interstitial
• Nocturnal dyspnea spaces and alveoli.
• Cool, pale skin • The fluid within the alveoli mixes with air, producing
Causes of Right sided HF the classis sign of pulmonary edema---frothy pink
• Left-sided heart failure (blood-tinged sputum)
• Hypertension • The large amount of alveolar fluid creates a
• Age, infiltration, infections, that cause cardiac wall diffusion block that severely impairs gas exchange -
stiffness Hypoxemia
• Heart valve disorders
• Lung disorders: COPD and Pulmonary Embolism Causes
• Left-sided heart failure
Clinical manifestations: Right-sided heart failure • Left-sided myocardial infarction (MI)
• enlarged liver (hepatomegaly) • Valvular heart disease
• enlarged spleen (splenomegaly) • Arrhythmias
• epigastric tenderness • High blood pressure
• ascites
• edema Clinical Manifestations
• anorexia, fullness, nausea • Scared expression on client’s face
• Jugular venous distension (JVD) • Shortness of breath
• increased Weight • Orthopnea
• nocturia • Rapid, labored breathing
• Tachycardia
Diagnostic Exam • Dependent crackles developing into diffuse crackles
• Electrocardiography • Signs and symptoms of shock: cold, clammy skin;
• Chest x-ray low blood pressure
• Frothy, blood stained sputum with cough; looks like
BNP level: increased beaten egg-whites (PINK FROTHY-SPUTUM)
• Echocardiogram • Cyanosis
• Jugular vein distension
Treatments for HF • Respiratory acidosis
• Goal is to decrease workload on the heart. • Restlessness
• Diuretics • S3 gallop
• ACE inhibitors: dilate blood vessels decreasing • Cardiomegaly
workload of heart.
• Angiotensin II receptor blockers: can be used in Diagnostic Exam
place of ACE inhibitors. • Arterial Blood Gas
• Beta-blockers: slow the heart rate; prevent • Chest x-ray
remodeling. • Pulse oximetry
• Vasodilators: cause blood vessels to dilate. • Electrocardiography
• Positive inotropic drugs: makes the heart muscle
contract more forcefully. Treatments
• Anticoagulants: prevent clot formation. • Supplemental oxygen
• Opioids: relieve anxiety and decrease the workload • Elevate the head of the bed; lower foot of bed so
on the heart especially in pulmonary hypertension. fluid will pool in lower extremities
• Oxygen therapy: improves oxygenation. • Weigh daily to monitor for fluid retention.
• Lifestyle modification: exercise; weight loss; reduced • Strict I & O
• Sodium, alcohol, and fat intake; smoking cessation; • Treatment of underlying cause of cardiac condition.
stress reduction to reduce symptoms of heart • Consider mechanical ventilation.
failure. • Diuretics
• Coronary artery bypass surgery or angioplasty: for • Positive inotropic drugs
heart failure due to coronary artery disease (CAD). • Nitroglycerin
• Dobutamine IV

PULMONARY EDEMA – abnormal accumulation of fluid Cardiogenic shock - called pump failure
in the lungs. The fluid may accumulate in the interstitial • Condition of diminished cardiac output that
spaces or in the alveoli. severely impairs tissue perfusion.
• can happen because of a damaged muscle, poor
ventricular filling, or poor outflow from the heart. Note: *Biopsy
• As cardiogenic shock progresses, the vital organs
begin to lose perfusion until the heart is no longer Complications:
able to perfuse itself! • Coronary artery puncture
• Cardiogenic shock following acute MI means that • Myocardial trauma
the heart is too damaged to effectively perfuse • Dysrhythmias
itself. When this happens, the heart cannot eject • Pleural laceration
blood forward, and the ischemic heart muscle • Gastric puncture
cannot continue to function effectively. In the
presence of ischemia, the heart begins to beat Cardiac arrest - The heart is unable to pump and
erratically and cardiac output falls drastically. circulate blood to the body’s organs and tissues

Causes Pulseless Electrical Activity (PEA) - Occurs when

• Myocardial infarction electrical activity is present on the ECG but cardiac
• Lethal ventricular arrhythmias contractions are ineffective
• End-stage congestive heart failure
Clinical Manifestations
Signs and symptoms • In cardiac arrest, consciousness, pulse and blood
• Tachycardia pressure are lost IMMEDIATELY.
• Hypotension • Breathing usually ceases, but ineffective respiratory
• Cool clammy skin gasping may occur.
• Diaphoresis • Dilated pupils
• Cyanosis of lips and nail bed • Seizures
• Pallor
Diagnostic Exam • Cyanosis
• Serum enzymes • Irreversible brain damage
• ABGs: metabolic and respiratory acidosis and
hypoxia. Emergent Management
• Cardiac catheterization and echocardiography: • CPR
reveal other conditions that can lead to pump • Defibrillator
dysfunction and failure like cardiac tamponade, • High Quality Cardiopulmonary Resuscitation
pulmonary emboli, and hypovolemia. • Defibrillator
• Electrocardiography
--------------------------------------------------------------------------
Treatments --------------------------------------------------------------------------
• Maintenance of patent airway; preparation for
intubation and mechanical ventilation: prevent or FLUIDS AND ELECTROLYTES: BALANCE AND
manage respiratory distress. DISTURBANCE
• Supplemental oxygen •Fluid and electrolyte balance is essential to your
• IV fluids, crystalloids, colloids, or blood products: to body’s homeostasis.
maintain vascular volume.
• Vasopressors: reduce left ventricle workload. Body Fluids
• Inotropics: increase heart contractility and cardiac •Refers to body water in which electrolytes are
output. dissolved.
•Been described as “a sea within”
THROMBOEMBOLISM •Water is the largest single constituent of the body,
• Causes (cardiac in origin) representing 45% - 75% of the body weight
- Intracardiac thrombus
- atrial fibrillation FACTORS THAT INFLUENCE AMOUNT OF BODY FLUIDS
- Mural thrombi • Age
• Deep vein thrombosis (DVT) • Gender
• Body fat
PERICARDIAL EFFUSION AND
CARDIAC TAMPONADE

Pericardial effusion refers to the accumulation of fluid

in the pericardial sac.

Diagnostic Exam
• Echocardiogram
• Chest x-ray

Management: Pericardiocentesis
Functions of Body Fluids • Phosphates and sulfates – primary anions in
• Transport nutrients to the cells and carries waste the ICF
products away from the cells.
•Maintains blood volume. General Functions of electrolytes:
•Regulates body temperature.  promote neuromuscular irritability
•Serves as aqueous medium for cellular metabolism.  maintain body fluid volume and osmolality.
•Assists in digestion of food through hydrolysis.  distribute body water between compartments
•Acts as solvents in which solutes are available for cell  regulate acid-base balance
function.
•Serves as medium for the excretion of waste products. Movements of Water and Electrolytes
1. PASSIVE TRANSPORT
a. Diffusion
Body fluids are distributed in the body in two b. Osmosis
compartments: c. Filtration
ECF subdivided further into: 2. ACTIVE TRANSPORT
I. Interstitial fluid
II. Intravascular fluid Passive transport
III. Transcellular a. Diffusion - movement of particles from an area of
higher to lower concentration within one
I. Intravascular - Fluid within blood vessels compartment.
• Contains plasma (3 L out of the average 6 L blood • occurs through the random movement of ions
volume) and molecules.
• particles will distribute themselves evenly.
II. Interstitial- Fluids that surrounds the cells (11 to 12 L) • an example is the exchange of O2 and CO2
Ex: lymph between the pulmonary capillaries and alveoli.

III. Transcellular b. Osmosis - movement of fluid from an area of lower

• 1-3% of body weight concentration to higher concentration across the semi-
• Approximately 1-2 L permeable membrane.
• Cerebrospinal fluid, pericardial fluid, synovial • normal serum osmolality is 280-300mOsm/kg.
fluid, pleural fluids • osmolality of ECF and ICF is always equal.
• Sweat
• Digestive secretions

Note:
• There is a continuous exchange of fluid between the
fluid compartment, of these spaces, only the plasma is
directly influenced by the intake or elimination of fluid
from the body.

• third-space fluid shift or “third spacing” where there Important terms:

is a loss of ECF into a space that does not contribute to
the equilibrium between ICF and ECF.
“Third spacing” occurs in:
• ascites
• burns
• peritonitis
• bowel obstruction
• massive bleeding into a joint or body cavity.
ELECTROLYTES - Chemical compounds in solution that
have the ability to conduct an electrical current.
•They break into ions:
• Cations carry positive charges;
• Anions carry negative charges
Tonicity - is the ability of all the solutes to cause an
osmotic driving force that promotes water movement
from one compartment to another
Osmolality - reflects the concentration of fluid that
affects the movement of water between fluid
compartments by osmosis.
• Also measures the ability of a solution to create
osmotic pressure and affect movement of water.
(mOsm/kg)
Osmolarity - reflects the concentration of solutions.
(mOsm/L)
Oncotic pressure - is the osmotic pressure exerted by
proteins (ex.albumin)

• Sodium – primary cation in the ECF; important Osmotic diuresis - occurs when the urine output
in regulating fluid volume increases due to the excretion of substances such as
• Chloride – primary anion in the ECF glucose, mannitol, or contrast agents in the urine.
• Potassium – primary cation in the ICF
c. Filtration - is the process by which water and • Pumps and carries fluids and other good stuff
diffusible substances move together in response to throughout the body, to the vital organs, especially to
fluid pressure. This process is active in capillary beds. the kidneys

• an example is the passage of water and electrolytes Pituitary gland

from the arterial capillary bed to the interstitial fluid. • antidiuretic hormone (ADH), which causes retention
of water.
Hydrostatic pressure - blood entering the capillaries
does so at a pressure greater that the interstitial Parathyroid glands
pressure, so fluid and solutes move out of capillaries. • The parathyroid glands secrete parathyroid hormone
At the venous end of the capillary bed, hydrostatic (PTH).
pressure is less than the interstitial pressure and fluid
and waste products move back into capillaries. • This causes an increase in serum calcium by pulling it
from the bones and placing the calcium in the blood.
2. Active transport -movement of ions from an area of
lesser to greater concentration with an ion pump. Thyroid gland
• (Na –K pump) •The thyroid gland releases thyroid hormones.
• Providing energy
Concentration of Fluids • Increasing pulse rate
• Isotonic • Increasing cardiac output
• Hypotonic • Increasing renal perfusion
• Hypertonic • Increasing diuresis
• Ridding of excess fluid
Isotonic - Exerts the same osmotic pressure as that
found in plasma. Osmolarity is 240-340mOsm/L. Hypothalamus
• thirst response
Hypotonic - Exerts less osmotic pressure than that of • AGE matters
blood plasma. Osmolarity is less than 240 mOsm/L
Small intestine
Hypertonic - Exerts a higher osmotic pressure than that • absorbs 85% to 95% of fluid from ingested food
of blood plasma. Osmolarity is more than 340mOsm/L. • delivers it into the vascular system

REGULATION OF BODY FLUIDS AND ELECTROLYTES Lymphatic system

Kidneys • moves water and protein back into the vascular
• Daily urine volume: 1 to 2 L space
• Normal output should be 1 mL/kg/hr
How do we lose fluid?
Skin We lose fluid by 2 ways:
• Insensible water loss through the skin: 600 mL 1. Sensible
2. Insensible
Adrenal glands
• The adrenal glands secrete aldosterone. 1. Sensible fluid loss:
 loss that is SEEN
Aldosterone:  urine, sweat, and feces.
• Retains sodium and water.  Kidneys--800 to 1500 mL/day
• Excretes potassium at the same time.  NGT
•sodium and potassium have an inverse relationship.
• Builds up vascular volume, which makes the BP to 2. Insensible fluid loss:
increase • loss that is NOT SEEN
• Occurs through the intestinal tract, lungs, and
Remember, more vascular volume means more blood skin.
pressure. • Skin—water evaporation
• Lungs- approximately 500 mL/day
• GI-100 to 200 mL/day
Lungs
• The lungs regulate fluid by releasing water as vapor Abnormal fluid loss
with every exhalation. Every time you exhale, water is Abnormal fluid loss results from a physiologic
lost imbalances.
Examples include:
Gastrointestinal tract  Fever or an increased room temperature
• Usual loss is around 100 to 200 mL  Severe burns
 Hemorrhage
Cardiovascular system  Emesis
 Fistulas
  Secretions • Aldosterone:causes sodium and water retention
 Wound exudates while causing potassium excretion through the
 Paracentesis urine.
 Thoracentesis • PTH: increases urine excretion of phosphorus
 Diaphoresis and decreases urine excretion of calcium.

DEHYDRATION What causes decreased oral electrolyte intake?

The 2 types of dehydration are: • Anorexia
1. Mild dehydration - 2% loss of body weight, • Feeling weak
which equals 1 to 2 L of body fluid. • Shortness of breath
1. Marked dehydration - 5% loss of body weight, • GI upset
which equals 3 to 5 L of body fluid. • Income
• Fad dieting (low in potassium)
How do we measure electrolytes?
1. mg/dL (deciliter) - measures the weight of the Abnormal electrolyte losses
particle in a certain amount of volume. • Vomiting
• Nasogastric (NG) suction
2. mEq/L - milliequivalent is one-thousandth of an • Intestinal suction
equivalent • Drainage
• Paracentesis
• the amount of a substance that will react with a • Diarrhea
certain number of hydrogen ions. This is measured per • Diuretics
liter of fluid. Simply put, this is atomic weight. • Kidney trauma, illness,

3. mmol/L (millimoles/liter) - millimole is one- CASE IN POINT

thousandth of a mole per liter of fluid.
• Basically, this measurement offers an in-depth
analysis of the electrolyte being evaluated.
Where do electrolytes live in the body?
Electrolytes can be found all over the body.
1. Potassium: found inside the cell; the most
plentiful electrolyte in the body.
2. Magnesium: found inside the cell; second most
plentiful electrolyte in the body.
3. Sodium: numero uno electrolyte in the
extracellular fluid.
1. Phosphorus: found inside the cell and in the
bones.
2. Calcium: found mainly in bones and teeth;
some floats around in the blood as well.
3. Chloride: found inside the cell, the blood, and
the fluid between cells.
Hormones
Hormones help keep electrolytes within normal range.
A common nursing order is “nothing by mouth”
(NPO).
What causes electrolyte excess in the blood?
• Kidney trauma, illness, or disease
• Massive blood transfusions
• Tumors
• Crushing injuries
• Chemotherapy
Substances that can alter fluid balance
1. Plasma protein.
2. Glucose.
1. Plasma protein - holds on to fluid in the vascular
space. Albumin
CASE IN POINT
• If a client is badly burned, malnourished
(decreased protein intake), or has a disease
where the liver is not making adequate
amounts of albumin, problems can occur.

1. Insulin - moves potassium from the blood to the
inside of the cell, causing the serum K to drop.
2. Parathyroid hormone (PTH) - moves calcium from
the bone into the blood when serum calcium levels are
low.
• causes the serum calcium to increase.
3. Calcitonin - moves calcium into the bones as needed.
• When the serum calcium is too high, calcitonin
increases and moves calcium from the blood
into the bone.
• This causes serum calcium to decrease.
How do we get rid of excess electrolytes?
Excess electrolytes are excreted by:
• Urine, feces, and sweat.
• Adequate albumin needed to hold fluid in the
vessels may not exist; therefore, the fluid may
leak out of the vessels into the tissues and
cause shock.
2. Glucose - The vascular space likes the particle-to-
water ratio to be equal.
CASE IN POINT
• When the blood sugar is very high, as in
diabetics, the blood has too many glucose
particles compared to water in the vascular
space. This causes particle-induced diuresis
(PID), sometimes called osmotic diuresis.
-------------------------------------------------------------------------- • Excessive retention of water and sodium in the
-------------------------------------------------------------------------- extracellular fluid (ECF).
HYPERVOLEMIA AND HYPOVOLEMIA • Also called hypervolemia or isotonic
overhydration.
Fluid volume deficit (FVD) - results when fluid loss
exceeds fluid intake. Causes
• Renal failure
• sodium and water are lost in equal amounts from • CHF
the vascular space. • Cushing syndrome
• Excessive sodium: from IV normal saline or
• Also called hypovolemia or isotonic dehydration. lactated ringers(iatrogenic)or foods
*Not the same as dehydration • Blood product administration
• Increased ADH
What causes it? • Medications
• Decreased intake or poor appetite • Liver disease
• Drugs that affect fluids and electrolytes • Hyperaldosteronism
• Diuresis • Burn treatment
• Forgetting to drink and eat
• Poor response to fluid changes Signs and symptoms
• Vomiting • Jugular vein distension ( JVD)
• Diarrhea • Bounding pulse, tachycardia
• GI suction • Abnormal breath sounds
• Diuretics • Polyuria
• Impaired swallowing • Decreased urine specific gravity
• Tube feedings • Dyspnea and tachypnea
• Fever • Increased BP
• Laxatives • Increased central venous pressure (CVP)
• Hemorrhage • Edema
• Third spacing • Productive cough
Signs and symptoms • Weight gain
• Acute weight loss Diagnostic tests and treatments
• Decreased skin turgor (tenting occurs) Tests:
• Postural hypotension (orthostatic hypotension) • Serum Electrolytes
• Increased urine specific gravity • BUN and Creatinine
• Weak, rapid pulse • Chest x-ray:
• Cool extremities • If the heart is enlarged, as can be seen
• Dry mucous membranes with an x- ray, this could mean
• Decreased BP congestive heart failure.
• Decreased peripheral pulses Treatments:
• Oliguria • Treat the cause
• Decreased vascularity in the neck and hands • Loop diuretics: Furosemide (Lasix)
• Decreased central venous pressure • Potassium-Sparing Diuretics: Spironolactone
• Increased respiratory rate (Aldactone)
• Dietary Sodium Restrictions
Diagnostic tests and treatments
Laboratory testing for FVD include: Complications
• serum electrolytes • CHF
• Hct • pulmonary edema
• Urine specific gravity
In fluid volume deficit and fluid volume excess, the
Treatment measures: osmolarity and serum sodium are not affected as the
 oral or IV fluid replacement client loses fluid and sodium proportionately.
 if is due to hemorrhage or blood loss---blood
products
Complications --------------------------------------------------------------------------
 Shock. --------------------------------------------------------------------------
 Poor organ perfusion, leading to acute tubular ELECTROLYTES
necrosis and renal failure.
 Multiorgan dysfunction due to poor perfusion. SODIUM
 Decreased cardiac output. Sodium imbalances
The following apply to the electrolyte sodium:
Fluid volume excess (FVE) - results when fluid intake • Chief electrolyte in ECF.
exceeds fluid loss.
• Assists with generation and transmission of nerve Treatment:
impulses. • Depends on the cause
• An essential electrolyte of the sodium– potassium • 0.9% normal saline IV
pump in the cell membrane. • 3% Saline
• Food sources: bacon, ham, sausage, catsup, mustard, • Watch for FVE
relishes, processed cheese, canned vegetables, bread, • Increased dietary Sodium
cereals, snack foods. • If appropriate, discontinue drugs/treatments
• Excess sodium is excreted by kidneys. that could be causing sodium loss.
• Excretion of sodium retains potassium.
• Normal adult sodium level is 135 to 145 mEq/L. COMPLICATIONS
• Helps maintain the volume of body fluids. • Seizures and brain damage are the major
• Sodium is the only electrolyte that is affected by complications associated with hyponatremia.
water. • Also, consider what caused the hyponatremia
• Sodium level decreases when there is too much when determining what could harm your
water in the body. patient.
• Conversely, sodium level increases with less water in
the body. Hypernatremia - serum sodium greater than 145 mEq/L

Renin–angiotensin system • similar to dehydration: there is too much sodium and

• ECF (vascular volume) decreased → Renin not enough water in the body.
produced by the kidneys →Angiotensin I
converted to angiotensin II →Aldosterone Causes
secreted → Sodium and water retained. • Anything that causes an increased “water” loss
• If sodium and water are retained or lost equally or excessive sodium intake can cause
then there will be no change in serum sodium. hypernatremia.
• Administration of IV normal saline without
Hyponatremia - Serum sodium less than 135 mEq/L. proper water replacement
• Hyperventilation
Hyponatremia is: • Watery diarrhea
• Not enough sodium in the ECF (vascular space). • Hyperaldosteronism
• Possibly, there is too much water diluting the • Renal failure
blood which makes serum sodium go down. • Heat stroke
• Anytime there is a sodium problem there is a • NPO status
fluid problem as well. • Infection
• Diabetes insipidus
Hyponatremia classification according to ECF volume • Tachycardia
level
• HYPOVOLEMIC HYPONATREMIA Signs and symptoms
• HYPERVOLEMIC HYPONATREMIA • Dry, sticky mucous membranes
• ISOVOLUMIC HYPONATREMIA • Thirst
• Changes in level of consciousness (LOC)
Causes • Decreased heart contractility
• Excessive administration of D5W • Seizure
• Diuretics • Muscle twitching
• Wound drainage • Muscle weakness
• Psychogenic polydipsia • Decreased DTRs
• Decreased aldosterone
• Low-sodium diet Diagnostic tests and treatments
• Syndrome of inappropriate antidiuretic • Tests:
hormone (SIADH) • serum electrolytes
• Vomiting and sweating • Treatment: individualized/specific depending on
• Replacing fluids with water only the cause.
• Muscle weakness • Restrict all forms of sodium: Foods can have
excess sodium as well as drugs and IV fluids.

Signs and symptoms COMPLICATIONS

• Decreased deep tendon reflexes (DTRs) • As with hyponatremia, seizures and brain
• Diarrhea damage are the major complications associated
• Respiratory problems with hypernatremia.

Diagnostic tests and treatments POTASSIUM

Tests: Potassium imbalances
• hyponatremia is serum electrolytes
 • Makes skeletal and cardiac muscle work COMPLICATIONS
correctly. • life-threatening arrhythmias
• Major electrolyte in the intracellular fluid. • arrhythmias
• Potassium and sodium are inversely related - decreased cardiac output
(when one is up, the other is down). - resulting in hypotension.
• Plays a vital role in the transmission of electrical • Respiratory depression may also occur.
impulses.
• Food sources: peaches, bananas, figs, dates, Hyperkalemia - serum potassium greater than 5.0
apricots, oranges, melons, raisins, prunes, mEq/L.
broccoli, potatoes, meat, dairy products. • In severe hyperkalemia, ascending flaccid
• Excreted by the kidneys. paralysis of the arms and legs may be seen;
• Stomach contains large amount of potassium. • this paralysis moves distal to proximal.
• Normal potassium level: 3.5 mEq/L to 5.0
mEq/L Causes
• Renal failure
Hypokalemia - serum potassium below 3.5 mEq/L • IV potassium chloride overload
• Paralytic ileus can occur from severe • Burns or crushing injuries
hypokalemia. • Tight tourniquets
• Abdominal distension • Hemolysis of blood sample
• muscle cramps • Incorrect blood draws
• muscle weakness • Salt substitutes
• Potassium-sparing diuretics
Causes • Blood transfusions
• Diuretics • ACE inhibitors
• Steroids • Tissue damage
• GI suction • Acidosis
• Vomiting • Adrenal insufficiency (Addison’s disease)
• Diarrhea • Chemotherapy
• NPO status; poor oral intake
• Age Signs and symptoms
• Cushing syndrome • Begins with (1)muscle twitching associated with
• Kidney disease tingling and burning; (2)progresses to
• Alkalosis numbness, especially around mouth;
• IV insulin (3)proceeds to weakness and flaccid paralysis

Signs and symptoms • Excess potassium interferes with skeletal and

• Muscular weakness, cramps, flaccid paralysis
• Hyporeflexia
• Life–threatening arrhythmias
• Slow or difficult respirations
• Weak, irregular pulse
• Decreased bowel sounds
• Decreased LOC
Diagnostic tests and treatments
Tests:
• serum electrolytes
• EKG (shows flattened T wave, depressed ST
segment, and a U-wave)
Treatments:
• determine the cause
• High potassium diet
• IV or oral potassium chloride
• check for proper kidney function or good urine
output.
• A good rule to remember when administering
IV K is not to exceed 20 mEq/hour.
• Clients taking a cardiac glycoside with a diuretic
should be monitored closely for hypokalemia,
which can potentiate the cardiac glycoside and
cause toxicity
• switched to a potassium-sparing diuretic
smooth muscle contraction, nerve impulse
conduction, acid–base balance, enzyme action,
and cell membrane function
• Diarrhea
• Smooth muscles of the intestines hyper
contract, resulting in increased motility
• Dysfunctional nerve impulse conduction and
smooth muscle contraction
• Cardiac arrhythmia;
- bradycardia; EKG changes: peaked T-wave, flat
or no P-wave, wide QRS complex; ectopic
beats on EKG leading to complete heart block,
asystole, ventricular tachycardia, or ventricular
fibrillation
Diagnostic tests and treatments
Tests:
• serum electrolytes
• ECG will also be assessed
Treatments:
• depends on the primary cause.
• IV insulin in conjunction with 10–50% glucose IV
(IV insulin will lower the serum K by pushing it
into the cell.
• Administration of sodium polystyrene sulfonate
(Kayexalate) with 70% sorbitol
 • Kayexalate---serum sodium as hypernatremia • Laryngeal spasm
can occur. • Hyperactive DTRs
• Diuretics to increase renal excretion of K. • Cardiac changes: decreased pulse, prolonged ST
• 10% calcium gluconate IV (to decrease interval, prolonged QT interval, decreased
myocardial irritability). myocardial contractility
• Hemodialysis • Calcium regulates depolarization in the cardiac
• Peritoneal dialysis cells. If calcium is decreased, depolarization is
• Limit high potassium foods. impaired
• Limit drugs which could cause retention of K • Respiratory arrest
(aldactone). • LOC changes
• Increased gastric activity
Complications
• monitor clients for dehydration, neurological Diagnostic tests and treatments
changes, and life-threatening arrhythmias. Tests:
• assess the electrolytes
• ECG may be performed
CALCIUM • dependent on the cause
Calcium imbalances • IV calcium
• Acts like a sedative on muscles. • heart monitor
• Most abundant electrolyte in the body. • Vitamin D therapy
• Has an inverse relationship to phosphorus. • Increase dietary calcium
• Necessary for nerve impulse transmission, Complications
blood clotting, muscle contraction, and • Seizures, laryngospasm, respiratory arrest, and
relaxation. arrhythmias
• Needed for vitamin B12 absorption.
• Promotes strong bones and teeth. Hypercalcemia - serum calcium level that exceeds 10.5
• Who needs extra calcium? -- Children, pregnant mg/dL.
women, lactating women. Food sources: milk, • If there is increased Ca in the blood, think that
cheese, dried beans. the muscles will be “sedated”
• Must have vitamin D present to utilize calcium.
• If blood levels of calcium decrease, the body Causes
takes calcium from the bones and teeth. (to • Decreased DTRs
build the blood level back up) • Muscle weakness
• Renal calculi
Parathyroid hormone (PTH) - increases serum calcium • Pathological fractures
by pulling it from the bones and putting it in the blood. • Central nervous system (CNS) depression:
Calcitonin - decreases serum calcium by driving the lethargy, coma, confusion
blood calcium back into the bones.
Signs and symptoms
• Normal calcium: 9.0 to 10.5 mg/dL • Early cardiac changes: increased P-wave;
decreased ST interval; wide T-wave; increased
Hypocalcemia - serum calcium level drops below 9.0 BP
mg/dL. • Late cardiac changes: decreased pulse moving
• When calcium is decreased, think “not to cardiac arrest
sedated.” • Respiratory arrest
• Decreased bowel sounds
Causes • Increased urine output
• Decreased calcium intake • Increased clotting times
• Kidney illness • Kidney stones
• Decreased vitamin D
• Diarrhea Diagnostic tests and treatments
• Pancreatitis Tests:
• Hyperphosphatemia • assess the serum electrolytes.
• Thyroidectomy • ECG
• Medications (calcium binders) • X-ray
• UTZ
• Urinalysis
Signs and symptoms Treatment:
• Muscle cramps • dependent on the cause
• Tetany • Normal Saline IV
• Convulsions • Excess calcium: think SEDATED
• Arrhythmias • IV phosphate
• Positive Chvostek’s sign
• Positive Trousseau’s sign Complication
 • Respiratory depression and arrhythmias • Administer of vitamin D preparations such as
calcitrol (rocaltrol)
PHOSPHORUS • Administration of phosphate-binding gels
Phosphorus imbalances • Restriction of dietary phosphorus
• Promotes the function of muscle, red blood • Possibly dialysis
cells (RBCs), and the nervous system.
• Assists with carbohydrate, protein, and fat Complications
metabolism. • Seizures, laryngospasm, respiratory arrest, and
• Food sources: beef, pork, dried peas/beans, arrhythmias
instant pudding.
• Has an inverse relationship with calcium. MAGNESIUM
• Regulated by the parathyroid hormone. Magnesium imbalances
• Normal phosphorus is 3.0 to 4.5 mg/dL. • Present in heart, bone, nerves, and muscle tissues.
• Remember that phosphorus and calcium have • Second most important intracellular ion.
an inverse relationship! • Assists with metabolism of carbohydrates and
proteins.
Hypophosphatemia - serum phosphate that is below • Helps maintain electrical activity in nerves and
3.0 mg/dL. muscle.
• Also acts like a sedative on muscle.
Causes • Food sources: vegetables, nuts, fish, whole grains,
• Hypophosphatemia looks just like peas, beans.
hypercalcemia. • Magnesium levels are controlled by the kidneys
(excreted by kidneys).
Signs and symptoms • Normal magnesium: 1.3 to 2.1 mEq/L.
• Hypophosphatemia looks just like • Can cause vasodilatation.
hypercalcemia. • The majority of magnesium comes from our dietary
intake.
Diagnostic tests and treatments
Tests: Hypomagnesemia - serum magnesium level below 1.3
• Serum electrolytes mEq/L.
• X-ray
Causes
Treatment: • Diarrhea
• Supplemental Phosphorus • Diuretics
• IV phosphorus is given when phosphorus drips • Decreased intake
below 1 mg/dL and when the GI tract is • Chronic alcoholism
functioning properly • Medications
• Additional treatments depend on the • Decreased magnesium levels increase nerve
underlying cause. impulses. Think: NOT SEDATED.

Complication
• respiratory depression and arrhythmias Signs and symptoms
• Increased neuromuscular irritability
Hyperphosphatemia - serum phosphate level that is • Seizure
above 4.5 mg/dL. • Hyperactive DTRs
• Laryngeal stridor
Causes • Positive Chvostek’s and Trousseau’s signs
• Hyperphosphatemia looks just like • Cardiac changes: arrhythmias; peaked T-waves;
hypocalcemia. depressed ST segment; ventricular tachycardia;
ventricular fibrillation; irregular heartbeat
Signs and symptoms • The heart is a smooth muscle. If there is not
• Hyperphosphatemia looks just like enough magnesium to sedate it, impaired nerve
hypocalcemia. conduction and muscle spasms can occur
• Dysphagia
• Decreased GI motility
• Changes in LOC

Diagnostic test and treatments Diagnostic tests and treatments

Tests: Tests:
• check electrolyte levels. • assess the serum electrolytes.
• X-ray • Urinalysis
• ECG
Treatment:
• underlying cause must be treated
 • New diagnostic tests include nuclear magnetic • Inverse relationship with bicarbonate
resonance spectroscopy and ion-selective • HYPERCHLOREMIC METABOLIC ACIDOSIS
electrode tests
Causes
Treatment: • Excessive Cl intake
• underlying cause must be identified and • Renal Tubular Necrosis
treated. • DHN
• Increased dietary magnesium • Excessive reabsorption of Cl from GI tract
• Magnesium salts • Excessive intake of NaCl with water loss
• Magnesium sulfate IV • Hypernatremia

Complications Assessment Findings

• Laryngospasm. • Lethargy
• Aspiration due to dysphagia. • Drowsiness
• Arrhythmias. • Weakness
• Dyspnea
Hypermagnesemia - serum magnesium level above 2.1 • Tachypnea
mEq/L. • Headache
• Remember magnesium acts like a sedative.
“THINK SEDATED” with hypermagnesemia. Diagnostic Findings and Treatments
• Serum Cl (electrolyte)
Causes • Serum Na (electrolyte)
• Renal failure • Fluid administration
• Increased oral or IV intake • Restricted Na and Cl intake
• Antacids

Signs and symptoms --------------------------------------------------------------------------

• BP decreases
• Facial warmth and flushing
• Drowsiness to comatose state depending on
severity of imbalance
• Decreased DTRs
• Generalized weakness
• Decreased respirations to respiratory arrest
depending on severity of imbalance
• Cardiac changes: decreased pulse, prolonged
PR, wide QRS, cardiac arrest
Diagnostic tests and treatments
Tests:
• serum electrolytes
• ECG
Treatments:
• depends on the primary cause
• Decrease magnesium salt administration
• If in an emergency situation, respiratory
support may be needed
• Hemodialysis with magnesium free dialysate
• Loop diuretics
• 0.45% saline solution and/or IV calcium
gluconate to help balance the magnesium
levels.
--------------------------------------------------------------------------
ACID-BASE BALANCE
Respiratory acidosis and alkalosis overview
• carbon dioxide---an acid
• carbon dioxide + water =carbonic acid.
• get rid of carbon dioxide àexhaling
Lungs: carbon dioxide.
• In an acid–base imbalance such as respiratory acidosis or
alkalosis, the lungs are sick.
• compensating organs: kidneys
- manipulating the chemicals bicarbonate and
hydrogen to correct the imbalance and bring
the pH back into normal range
- This is done by secreting bicarbonate and
excreting hydrogen.
Kidneys: slow but effective
Metabolic acidosis and alkalosis overview
• Kidneys: ORGANS in metabolic acidosis and
metabolic alkalosis
• Bicarbonate and hydrogen are considered the
problem chemicals when the kidneys are sick.
• compensating organs: lungs
• Lungs can blow off or retain carbon Dioxide quickly

Complications NORMAL VALUES:

• arrest, cardiac arrest, and hypotension. • pH level: 7.35 – 7.45
• PaCO2: 35- 45 mmhg
• HCO3: 22 – 26 mmhg

Respiratory acidosis
CHLORINE
• An acid–base imbalance that occurs when the pH is
HYPERCHLOREMIA - Excess Chloride in the ECF
decreased, partial pressure of carbon dioxide
• Serum Cl level: greater than 106 mEq/L (PCO2) is increased—greater than 45 mm Hg.
• Hyperchloremia is associated with
hypernatremia • When you hypoventilate…?
 Carbon dioxide builds up in the blood: Hypercapnia--
buildup of carbon dioxide in the blood to levels greater than
45 mm Hg.
Causes
• respiratory acidosis: “breathing”
• Decreased alveolar ventilation: carbon dioxide
retention
• Anytime poor gas exchange exists, CO2 builds up in
the bloodà Respiratory acidosis
• Respiratory arrest
• Some drugs (narcotics, sedatives hypnotics,
anesthesia, ecstasy)
• Sleep apnea
• Excessive alcohol
• Surgical incisions (especially abdominal), broken ribs
• Collapsed lung (pneumothorax, hemothorax)
• Weak respiratory muscles (myasthenia gravis,
Guillain–Barré syndrome)
• Airway obstruction (poor cough mechanism,
laryngeal spasm)
• Brain trauma (specifically medulla)
• High-flow O2 in chronic lung disease
• Severe respiratory distress syndrome
Signs and symptoms
Vary depending on the initial cause:
• Neurological changes: headache, confusion, blurred
vision, lethargy coma,
• Papilledema
• Hyperkalemia
• Decreased muscle tone; decreased DTRs
• Acute respiratory acidosis causes hyperkalemia.
With chronic respiratory acidosis, the K+ may be
normal as the kidneys have time to readjust and
get the K+ back into the normal range.
• Hypotension
• Restlessness; tachycardia
• Arrhythmias
• Cardiac arrest
• Acidic urine
• Warm skin
Diagnostic tests and treatments
• Treat the cause.
• Airway clearance: possible intubation.
• Administer drugs to open up the airways and thin
out secretions so they can be coughed up.
• Increase fluids to liquefy secretions so they can be
coughed up more easily.
• Oxygen therapy.
• Respiratory therapy: breathing treatments.
• Elevate head of bed (HOB) for lung expansion.
• Monitor ABGs.
• Monitor for electrolyte imbalances.
• Monitor pulse oximetry.
• Administration of Pulmocare: a tube feeding
sometimes used to decrease CO2 retention.
MORE ON OXYGEN THERAPY
• low-dose oxygen-- chronic lung conditions
• high dose oxygen– acute lung conditions
What do the ABGs look like?
• pH: Less than 7.35
• PaCO2: Greater than 45 mm Hg
• PaO2: Less than 80 mm Hg
• HCO3: Normal until kidney compensation starts;
then will start to rise above 26 mEq/L
What can harm my client?
• Respiratory arrest.
• Arrhythmias: leading to cardiac arrest and shock.
• Severe decrease in LOC.
Recap of respiratory acidosis
• The name “respiratory” tips you off to the fact that a
lung problem exists
• Since it is a lung problem, the problem chemical is
the acid carbon dioxide
• Acidosis from a lung problem is due to irregular
breathing. Perhaps the client is hypoventilating—
breathing only 2 to 4 times a minute, causing
retention of carbon dioxide (CO2).
• Maybe the client has stopped breathing altogether
—possibly not exhaling carbon dioxide (CO2) at all.
The client retains all of this carbon dioxide (CO2),
which causes a buildup of acid in the body
• This buildup of acid causes the pH to decrease.
Respiratory Alkalosis
• an acid–base imbalance where the PaCO2 is less
than 35 mm Hg and the pH is greater than 7.45.
• Decrease PaCO2 in the blood: excessive exhalation
—hyperventilation.
• When the lungs are impaired, the kidneys
compensate with their own chemicals—
bicarbonate and H+.
• The kidneys will retain H+ because this is acid.
• The kidneys will excrete bicarbonate because this is
base/alkalotic.
• This excretion of the base will help raise acid levels
and restore the body to a normal pH.
• Respiratory alkalosis means that the client has lost
excessive CO2 (acid), thus making the client
alkalotic.
• Hypocapnia: occurs when the CO2 is low
Causes
• High altitudes
• Anemia
• Hypoxia
• Labor and delivery measures!
• Hysteria; anxiety
• High mechanical ventilator setting
• Aspirin overdose
• Fever
• Sepsis
Signs and symptoms
• Hyperventilation
• Light-headedness, dizziness fainting
• Rapid pulse
• Hypokalemia
• Arrhythmias
• Hypocapnia stimulates the autonomic nervous
system, which cause anxiety, changes in respiration,
tingling, and sweating.
• Calcium acts like a sedative. Hypocapnia decreases
serum calcium so the muscles may get tight. This
can lead to tetany and seizures!
Why do you breathe into the brown bag when you are
hyperventilating?
 To bring carbon dioxide back into our body
Diagnostic tests and treatments
• Treat the cause.
• Monitor vital signs, especially respirations.
 • Monitor electrolytes.
• Administer antianxiety medications as ordered.
• Place on mechanical ventilator to control respiratory
rate in severe cases.
• Monitor ABGs.
• Calm the client.
• Have client breathe into paper bag or rebreather
mask to encourage CO2 retention.
What do the ABGs look like?
• pH: Greater than 7.45 (alkalosis makes pH go up)
• PaCO2: Less than 35 mm Hg (because it is being
exhaled)
• PaO2: Greater than 100 mm Hg
• HCO3: Normal until kidney compensation starts;
then will be less than 22 mEq/L
Complications
• Life-threatening arrhythmias.
• Seizures.
Recap of respiratory alkalosis
• The name “respiratory” tips you off to the fact that a
lung problem exists
• Since it is a lung problem, the problem chemical is
the acid carbon dioxide (CO2)
• Excessive exhalation causes PaCO2 to decrease in
the blood. Acid is lost.
• When the lungs are impaired, the kidneys
compensate with their own chemicals—bicarbonate
and H+. The kidneys will retain H+ because this is
acid.
• We want to keep acid since the body is losing acid
from the excessive exhalation.
• The kidneys will excrete bicarbonate—a base—in
order to create a more acidic environment and
return the pH to normal
• Respiratory alkalosis means that the client has lost
excessive CO2 (acid), thus making the client alkalotic
Metabolic Acidosis
• An acid–base imbalance where the pH is less than
7.35 and the bicarbonate level is less than 22 mEq/L.
• Acid (H+ ions) builds up in the body, or too much
bicarbonate has been lost from the body.
• The less bicarb you have in the body, the more acid
you will be.
• Kidneys: Metabolic disorders
• Bicarbonate and H+
• The decrease in the alkaline substances (bases)
causes a build up of acids in the body, causing
acidosis.
• Lungs: compensate in just a few minutes
Causes
• Diabetic ketoacidosis, malnutrition, starvation
• Lactic acidosis
• Shock
• Kidney illness
• Gastrointestinal (GI) illness: diarrhea
• Drugs: Diamox, Aldactone
• Aspirin overdose
Signs and symptoms
• if renal failure is the initial cause, you will see signs
and symptoms related to renal failure;
• if diabetic, ketoacidosis is the initial cause
• Hyperkalemia
• Arrhythmias
• Increased respiratory rate
• Headache, decreased LOC, coma
• Muscle twitching and burning, oral numbness,
weakness, flaccid paralysis (severe hyperkalemia)
• A Kussmaul’s respiration is an increase in rate and
depth of respiration.
• When Kussmaul’s respirations are present, CO2 is
being blown off in increased amounts.
Diagnostic tests and treatments
• Monitor ABGs.
• Treat the cause.
• Monitor and manage hyperkalemia.
• Monitor and manage arrhythmias.
• Monitor and manage hypercalcemia.
• Administer sodium bicarbonate IV to decrease
acidity of blood.
• Monitor LOC closely.
• Administer lactated Ringers (LR) given IV to increase
base level.
• Institute seizure precautions (brain doesn’t like it
when the pH is messed up).
What do the ABGs look like?
• pH: Less than 7.35
• PaCO2: Will decrease to less than 35 mm Hg as it is
blown off
• PaO2: Normal
• HCO3: Less than 22 mEq/L
Sodium bicarbonate - should be used only as a quick,
temporary fix for increased acid levels and should be given
according to specific ABG values rather than generously as
we used to do in the past during code situations.
Complications
• Life-threatening arrhythmias.
• Cardiac arrest.
Recap of metabolic acidosis
• The problem is with the kidneys, not the lungs.
• Bicarbonate (base) and H+ (acid) are associated with
the kidneys.
• Metabolic acidosis can be caused by loss of
bicarbonate through diarrhea, and renal
insufficiency.
• The decrease in the alkaline substances (bases)
causes a buildup of acids in the body. It can also be
caused by diseases that increase acid levels (OFA)
• The lungs compensate increasing respiratory rate
and depth to blow off CO2 and increase pH. This is
called a Kussmaul’s respiration.
Metabolic alkalosis
• an acid–base imbalance where the pH is greater
than 7.45 and the bicarbonate level is greater than
26 mEq/L.
• There is an excess of base in the body and a loss of
acid.
• Basically, pH is increased and bicarbonate is
increased.
• Metabolic: kidneys, which involve bicarbonate and
H+.
• The lungs compensate by retaining CO2 by means of
hypoventilation.
• This compensates for the alkalosis and helps the pH
go down into normal range.
Causes
 • Vomiting; bulimia; nasogastric (NG) tube suctioning • By monitoring your client’s carbon dioxide,
• Excess antacid ingestion bicarbonate, and pH levels you can successfully
• Blood transfusions prevent and treat any acid–base imbalances.
• Sodium bicarbonate • Acidosis: Think hyperkalemia and hypercalcemia.
• Thiazide and loop diuretics • Alkalosis: Think hypokalemia and hypocalcemia.
• Baking soda
• Hypokalemia ----------------------------------------------------------------------------------
• Activation of renin–angiotensin system ----------------------------------------------------------------------------------
• Steroids
• Dialysis
• Licorice

Signs and symptoms

• Arrhythmias, flattened T-wave
• Decreased respirations, hypoventilation
• Hypokalemia
• Tightening of muscles, tetany, LOC changes,
seizures, tingling in fingers and toes
• LOC changes
• Hepatic encephalopathy

What do the ABGs look like?

• pH: Greater than 7.45
• PaCO2: Normal; increases with compensation
• PaO2: Remains the same
• HCO3: Greater than 26 mEq/L

Diagnostic tests and treatments

• Treating the cause of the acid–base imbalance
(antiemetics for vomiting, etc.).
• Monitoring ABGs for further complications.
• Treating arrhythmias.
• Stopping client bicarbonate intake.
• Monitoring potassium levels and correcting
hypokalemia.
• Monitoring respirations and LOC.
• Assessing for hypotension.
• Treating dehydration if present.
• Assessing DTRs.
• Administering ammonium chloride IV in severe cases
to increase acidity (increases H+).
• Administering acetazolamide (Diamox) to increase
excretion of bicarbonate through the kidneys.

Complications
Metabolic alkalosis can cause the following life- threatening
illnesses:
• Arrhythmias.
• Cardiac arrest.
• Seizures.

Recap of metabolic alkalosis

• The problem is with the kidneys, not the lungs
• Bicarbonate (base) and H+ (acid) are associated with
the kidneys
• Metabolic alkalosis can be caused by increased
bicarbonate through diuretic therapy, prolonged
nasogastric suctioning, and excessive vomiting,
resulting in ↑ pH levels
• The lungs compensate by retaining CO2 by means of
hypoventilation. This compensates for the alkalosis
• Metabolic alkalosis is the most common acid– base
imbalance.
• It accounts for 50% of all acid–base disturbances.

SUMMARY
• The respiratory and renal systems can be both the
cause and “cure” for pH imbalances.
• Remember that the lungs control carbon dioxide
levels and the kidneys control bicarbonate levels.