PRELIM: NCM 112 LEC *Weak pulse, low-pitched, rumbling *RV failure

diastolic murmur
#1 VALVULAR HEART DISEASES
*Atrial dysrhythmias
• Regurgitation – backward flow of blood through a heart valve. Aortic Regurgitation *Diastolic murmur (High-pitched) *LV dilation and hypertrophy
• Stenosis – narrowing or obstruction of a valve’s orifice. @ 3rd or 4th ICS, left sternal *LV failure
• Prolapse – stretching of an AV valve leaflet into the atrium during systole. border
*Widened PP
MITRAL VALVE PROLAPSE – a portion of one or both mitral valve leaflets balloonsback into *Corrigan’s pulse
the atrium during systole. Aortic Stenosis *Asymptomatic *LV dilation and hypertrophy
*Low BP & PP *LV failure
• Cause:
*Systolic crescendo-decrescendo
→ inherited connective tissue disorder causing an enlargement of the mitral valve
murmur over the aortic area S4
leaflet/s.
heart sound
→ usually, asymptomatic
→ mitral click (extra heart sound)/murmur: often the first & only sign of MVP
AORTIC REGURGITATION – the flow of blood back into the left ventricle from the aorta during MEDICAL MANAGEMENT:
diastole.
✓ Monitor for dysrhythmias
→ Inflammatory lesions that deform the leaflets of the aortic valve; infective or rheumatic ✓ Eliminate caffeine and alcohol
endocarditis, congenital abnormalities, aneurysm, blunt chest trauma, deterioration of ✓ Stop smoking
an aortic valve replacement ✓ Give antidysrhythmic
→ Leads to left ventricular failure ✓ Vasodilators (aortic regurgitation): Cachannel blockers, ACE inhibitors, hydralazine
→ High-pitched, diastolic murmur at 3rd or 4th ICS at the left sternal border ✓ Same as with right or left ventricular failure
→ Widened pulse pressure ✓ Valve repair (valvuloplasty)
→ Water-hammer (Corrigan’s) pulse ▪ Commissurotomy (for mitral stenosis)
▪ Annuloplasty – for regurgitation
▪ Chordoplasty – for stretched, torn, or shortened chordae tendinae
✓ Valve replacement

MITRAL REGURGITATION – blood flows back from left ventricle into the left atrium during
systole.

• Causes:
→ degenerative changes, ischemia of the left ventricle, rheumatic heart disease,
myxomatous changes, infective endocarditis, collagen-vascular diseases,
cardiomyopathy, ischemic heart disease
→ Left atrium eventually hypertrophies and dilates, lungs become congested
→ Systolic murmur (high-pitched, blowing sound)

AORTIC STENOSIS – narrowing of the orifice between the left ventricle and the aorta.

• Causes:
→ Degenerative calcification, congenital leaflet malformations, rheumatic endocarditis
→ Asymptomatic
→ Leads to left ventricular failure
→ BP and pulse pressure may be low
→ systolic crescendo-decrescendo murmur over the aortic area, S4 heart sound;
vibration felt over base of heart

MITRAL STENOSIS – obstruction of blood flowing from the left atrium into the left ventricle.

• Causes:
→ rheumatic endocarditis
→ Also leads to left atrial hypertrophy, pulmonary congestion and right ventricular
failure
→ Symptoms develop with 1/3 to ½ reduction of valve opening (1st: dyspnea on
exertion)
→ Poor ventricular filling ⇢ ⇩ CO ➢Low-pitched, rumbling diastolic murmur, atrial
dysrhythmias
MANIFESTATIONS COMPLICATIONS
Mitral Valve Prolapse *Usually, asymptomatic
*Mitral click
Mitral Regurgitation *Systolic murmur (high-pitched) *LA dilation and hypertrophy
*Dyspnea *Pulmonary congestion
*Fatigue *RV failure
*Weakness
Mitral Stenosis *dyspnea on exertion – 1st *LA dilation and hypertrophy
symptom *Pulmonary congestion
NURSING MANAGEMENT:

✓ Teach pt about the diagnosis, the progressive nature of the d/o, and the treatment plan
✓ Prophylactic antibiotic therapy before undergoing invasive procedures
✓ Minimize risk for infectious endocarditis:
▪ Good oral hygiene
▪ Routine dental care
▪ Avoid body piercing
▪ Don’t use toothpicks/sharp objects into oral cavity
✓ First-degree relatives may be advised to have echocardiograms
✓ Mitral stenosis: anticoagulants
✓ avoid strenuous activities, competitive sports, and isometric exercise

✓ monitor v/s, heart and lung sounds

✓ palpate peripheral pulses
✓ assess for s/s of heart failure, dysrhythmias, angina
✓ take weight daily, report gains of 2 lbs in a day or 5 lbs in 1 week
✓ valvuloplasty and replacement:
▪ assess for s/s of emboli
▪ same care for post-procedure cardiac catheterization or PTCA
▪ medications for BP regulation, dysrhythmias
✓ patient teaching on diet, activity, medications, and self-care
✓ educate about long-term anticoagulant therapy – warfarin or aspirin
✓ doppler echocardiograms performed 3-4 wks from discharge
 #2 INFECTIOUS DISEASES OF THE HEART a) Penicillin CLINICAL MANIFESTATIONS:
b) Erythromycin
RHEUMATIC ENDOCARDITIS 1. Fever
c) Salicylates
2. Heart murmur (1⁰)
ACUTE RHEUMATIC FEVER: b. Steroids + cardiac glycosides and diuretics
3. Petechiae
c. Bed rest until lab studies return to normal
- May develop after an episode of group A beta-Hemolytic streptococcal d. Prophylaxis for valvular heart disease, bacterial endocarditis (esp. before
infections surgery and dental work)
PREDISPOSING FACTORS: NURSING DIAGNOSES:
→ School-aged children (5-15 years old) 1. Pain related to swelling of joints and liver enlargement
→ Family history of the disorder 2. Risk for non-compliance with drug therapy related to lack of knowledge about
→ Overcrowding importance of long-term therapy
→ Low socioeconomic status 3. Activity intolerance related to reduced cardiac reserve and fatigue
→ Malnutrition 4. Imbalanced nutrition: less than body requirements related to loss of appetite 4. Oslers nodes (small, painful nodules in the pads of fingers or toes)
→ Poor hygiene
NURSING INTERVENTIONS:
→ Previous history of the infection
1. Carditis
MOST SERIOUS COMPLICATION: RHEUMATIC HEART DISEASE
a. Penicillin
- As evidenced by: b. Bed rest until ESR is normal
→ Valvular disorders 2. Arthritis
→ Cardiomegaly a. Aspirin
→ Pericarditis b. Position child slowly
→ Heart failure 3. Chorea
→ Heart murmur a. Decrease stimulation
5. Janeway lesions (irregular, red or purple, painless flat macules in the palms,
˗ Jones Criteria: 2 major criteria or 1 major and 2 minor criteria b. Safe environment
fingers, hands, soles and toes)
- Major Criteria: c. Small, frequent meals
1. Carditis – inflammation of the three layers of the heart d. Sedatives
✓ Heart murmur 4. Nodules and rash: none
✓ Pericarditis with a rub 5. Alleviate child’s anxiety
✓ Cardiomegaly – enlarged heart 6. Provide age-appropriate sedentary play
✓ Heart failure 7. Provide client teaching and discharge planning:
2. Migratory polyarthritis – inflammation of more than one joint and moves a. Adaptation of home environment to promote bedrest
from joint to joint (classic presenting manifestation of RF) b. Importance of prophylactic medication regimen
3. Sydenham’s chorea (St. Vitus Dance) – disorder of the CNS c. Diet modification in relation to decreased activity/ cardiac demands
˗ sudden, aimless, erratic, jerky, uncoordinated involuntary ▪ High CHON, high CHO
movements ▪ Vitamin & mineral supplements maintain hydration
˗ Onset: gradual, insiduous (starts with personality changes and d. Avoid reinfection
clumsiness) ˗ prompt dental care 6. Roth spots (hemorrhages with pale centers in the fundi of the eyes – caused
˗ Duration: 1-3 months ˗ prophylaxis before dental procedures by emboli)
4. Subcutaneous nodules – round, firm, free moving nodules over bony ˗ avoid people with URTI or strep infection
surfaces and tendons ˗ notify AP if the ff occurs:
5. Erythema marginatum – transient, non-pruritic rash starting with central ✓ Fever
red patches that expand - Results in series of irregular patches with red, ✓ Chills
raised margin and pale centers (giraffe spots) ✓ Sore throat
- Minor Criteria: ✓ Enlarged, painful lymph nodes
1. Fever e. Monitor for s/s of complications
2. Recent history of strep infection INFECTIVE ENDOCARDITIS:
3. Arthralgia – joint pain 7. Splinter hemorrhages (reddish-brown lines and streaks under the fingernails
4. Abdominal pain - A microbial infection of the endothelial surface of the heart and toenails)
5. Malaise, anorexia - Usually develops in people with prosthetic heart valves or structural heart
defects
DIAGNOSTIC TESTS: - Characterized by: Formation of vegetations on the heart valve
a. Elevated ESR (inflammation & infection) 2 TYPES:
b. Elevated C-reactive protein (inflammation; necrosis)
c. Antistreptolysin O (ASO) titer increased (N⁰= 0 – 200 iu) 1. Acute bacterial endocarditis
d. Positive throat culture 2. Sub-acute endocarditis
e. Leukocytosis
RISK FACTORS:
f. Changes in ECG (prolonged PR interval) 8. Cardiomegaly (An enlarged heart, isn't a disease, but rather a sign of another
✓ Prosthetic heart valves condition.)
MEDICAL MANAGEMENT: Goals
✓ Sructural cardiac defects 9. Heart failure
1. Identify and eradicate the causative organism and prevent complications ✓ Hx of bacterial endocarditis 10. Tachycardia
2. Maximize cardiac output ✓ Reduced immunologic response
3. Promote comfort ✓ Immunosuppressive therapy (fungal endocarditis)
4. Prevent complications ✓ Older people
a. Drug therapy
CNS MANIFESTATIONS: headache, transient cerebral ischemia, and strokes MYOCARDITIS:

ASSESSMENT AND DIAGNOSTIC FINDINGS: - The inflammation of the myocardial wall

- Frequently, the inflammation is not limited to the myocardium but extends
• Definitive diagnosis: when a microorganism is found in 2 separate blood
to the pericardium (pericarditis)
cultures, in a vegetation, or in an abscess
▪ Leukocytosis ETIOLOGY AND RISK FACTORS: in most cases, it is caused by viral infections
▪ Anemia
▪ Coxsackie virus (most common)
▪ Positive rheumatoid factor – antiglobulin antibodies often found in the
▪ Mumps
serum of patients with a clinical dx of RA
▪ Influenza
▪ Increased ESR or C-reactive protein
▪ Rubella
▪ Microscopic hematuria
▪ Measles
▪ Doppler echocardiography – mass on the valve, or supporting structures;
▪ Bacterial, fungal, helmintic, protozoal infections
identifies vegetations, abscesses, new prosthetic valve dehiscence, or new
▪ Alcohol
regurgitation
▪ Large doses of radiation therapy to the chest
PREVENTION:
CLINICAL MANIFESTATIONS:
1. Antibiotic prophylaxis (surgery & dental work)
• history of recent upper respiratory or GIT infection
- Amoxillin (Amoxil) 2g orally 1 hour before procedure (dental, surgical,
• Most frequent manifestations are:
invasive dx, delivery)
▪ Fatigue
- Clindamycin (Cleocin)
▪ Dyspnea
- Cephalexin (Keflex)
▪ Palpitations
- Cefazolin (Ancef, Kefzol)
▪ Chest pain (sharp, stabbing precordial pain)
- Ceftriaxone (Rocephin)
• ECG abnormalities
- Azithromycin (Zithromax)
- Clarithromycin (Biaxin) • Elevated serum levels of cardiac enzymes
2. Good oral hygiene • Chest X-ray may show an enlarged cardiac silhouette
3. Avoid nail biting • Elevated WBC and ESR
4. Avoid IUDs and body piercing and branding PREVENTION:
5. Ensure meticulous hand hygiene, site preparation and aseptic technique with
IV catheters and invasive procedures 1. Immunizations (influenza, hepatitis)
2. Early treatment
MEDICAL MANAGEMENT:
MEDICAL MANAGEMENT:
1. Antibiotic therapy – IV infusion for 2-6 wks
- DOC: Penicillin 1. Antibiotic therapy specific to the cause
2. Monitor temperature regularly 2. Bed rest
3. Limit physical activities for 6 months
SURGICAL MANAGEMENT INDICATIONS: 4. Avoid beta blockers – decrease the strength of ventricular contractions
a. Unresponsive to medications
b. Prosthetic heart valve endocarditis
c. Vegetation larger than 1 cm
d. Onset of complications (i.e. septal perforation)
1. Valve debridement or excision
2. Debridement of vegetations
3. Debridement and closure of abscess
4. Aortic or mitral valve debridement, excision or replacement

NURSING DIAGNOSES:

1. Decreased cardiac output related to cardiac valve dysfunction

2. Ineffective individual coping related to the chronic nature of the disease

NURSING MANAGEMENT:

1. Monitor temperature
2. Assess heart sounds
3. Monitor signs and symptoms of systemic embolization or pulmonary infarction;
organ damage (i.e., stroke), meningitis, HF, MI, glomerulonephritis and
splenomegaly
4. Assess daily invasive lines and wounds
5. Discharge teachings:
▪ Activity restrictions
▪ Continue medications as directed
▪ The need for antibiotic prophylaxis for invasive procedures
#3 ACUTE CORONARY SYNDROME (ACS) AND MYOCARDIAL INFARCTION (MI) MEDICAL MANAGEMENT: Goal

- To minimize myocardial damage, preserve myocardial function, and prevent

complications
ACUTE CORONARY SYNDROME:
A. Emergent Percutaneous Coronary Intervention
FORMS: B. Thrombolytics (Fibrinolytics)
C. Coronary artery bypass graft
• UNSTABLE ANGINA - While waiting:
▪ Reduced blood flow in a coronary artery 1. Elevate head/ loosen tight clothing
▪ angina/ preinfarction angina
2. Give O2
• Non-ST-SEGMENT ELEVATION MI 3. Gain IV access
▪ elevated cardiac biomarkers 4. Connect to heart monitor (or portable automatic external defibrillators)
▪ no definite ECG evidence of acute MI - Within 10 min:
• ST-SEGMENT ELEVATION MI 1. Admit to ER
▪ (+) ST segment elevation in 2 contiguous leads 2. Give aspirin
ASSESSING FOR ACS AND AMI:
DEFINITION OF TERMS: 3. Place on ECG monitor
• Cardiovascular 4. Draw blood samples of serum cardiac markers
▪ Atherosclerosis – characterized by yellowish plaques of cholesterol, other ▪ Chest pain A. Emergent Percutaneous Coronary Intervention (PCI)
lipids, and cellular debris in the inner layers of the walls of the arteries ▪ Increased jugular venous distention 1. Percutaneous Transluminal Coronary Angioplasty (PTCA)
▪ Plaque – a patch of atherosclerosis ▪ Increased BP 2. Intracoronary stent Implantation
▪ Atheroma – an accumulation of large amounts of extracellular lipids and ▪ Irregular pulse
fibrous tissue localized into a lipid core ▪ ECG changes 1. Percutaneous Transluminal Coronary Angioplasty (PTCA)
• Respiratory ˗ A balloon-tipped catheter is used to open the blocked coronary vessels
CORONARY ATHEROSCLOROSIS
▪ Shortness of breath, dyspnea, tachypnea, crackles to resolve ischemia
- Abnormal accumulation of lipid, or fatty substances and fibrous tissue in • Gastrointestinal ˗ Purpose: To improve blood flow within a coronary artery by copressing
the lining of the arterial blood vessel walls ▪ Nausea, indigestion and vomiting the atheroma
• Skin ˗ Can also be used to open blocked CABGs
▪ Cool, clammy, diaphoretic and pale appearance a. Coronary Artery Stent
• Neurologic ▪ Stent – a metal mesh that provides structural support to a vessel at
▪ Anxiety, restlessness and lightheadedness risk of acute closure
• Psychological ▪ May or may not be coated with medications
▪ Fear with feeling of impending doom ▪ Medication – coated stents:
▪ Denial Sirolimus (Rapamune)
Paclitaxel (Taxol)
Minimize the formation of thrombi or scar tissue within the
a. Unstable Angina: The patient has clinical manifestations of coronary coronary artery lesion
ischemia, but ECG and cardiac biomarkers show no evidence of acute MI b. Post-Procedure Care for PTCA
CLINICAL MANIFESTATIONS: b. STEMI: The patient has ECG evidence of acute MI with characteristic ▪ Monitor for signs of bleeding
changes; with significant to the myocardium ▪ GP IIb/IIIa agent (eptifebatide) several hours following PCI
• Chest pain c. NSTEMI: The patient has elevated cardiac biomarkers but no definite evidence ▪ Femoral sheaths removed after procedure by using a vascular
• Shortness of breath of acute MI closure device (Angio-Seal, VasoSeal)
• Indigestion
• Nausea
• Anxiety

ASSESSMENT AND DIAGNOSTIC FINDINGS:

• Patient history
▪ Description of presenting symptoms
▪ History of previous cardiac/ other illnesses
▪ Family history of heart disease
• Electrocardiogram (ECG)
▪ Hemostasis may also be achieved after sheath removal by:
- obtained within 10 min
Direct manual pressure
- T-wave inversion, ST-segment elevation and abnormal Q wave
Mechanical compression device (C-shaped clamp)
Pneumatic compression device (FemoStop)

▪ May return to the nursing unit with the large peripheral access
sheaths in place (removed after blood studies)
▪ Remain flat on bed
▪ Keep the affected leg straight until the sheaths are removed and for
a few hours afterwards
 ▪ Analgesics and sedation INDICATIONS:
▪ Back pain – reposition and heat application
˗ Alleviation of angina that cannot be controlled with medication or PCI
▪ IV atropine
˗ Treatment of left main coronary artery stenosis or multivessel CAD
▪ Unstable lesions and at high risk for abrupt vessel closure
˗ Prevention of and treatment for MI, dysrhythmias, or HF
restarted on heparin after sheath removal
˗ Treatment for complications from an unsuccessful PCI
IV infusion of GP IIb/IIIa inhibitor
Monitor closely CONSIDERATIONS FOR CABG:
May have delayed recovery period
▪ Hemostasis is achieved: ˗ Coronary arteries to be bypassed must have at least 70% occlusion or at least
˗ A pressure dressing is applied 50% occlusion if in the left main coronary artery
˗ Resume self-care ˗ The artery must be patent beyond the area of the blockage
˗ Ambulate unassisted ˗ Internal mammary artery should be used
B. Thrombolytics (Fibrinolytics) ˗ Commonly used vean: Saphenous vein (limited patency; 5 to 10 may have
▪ To dissolve the thrombus in a coronary artery atherosclerotic changes)
▪ Given within 30 min of presentation to the hospital (door-to-needle time) Traditional Coronary Artery Bypass Graft NURSING MANAGEMENT:
▪ Indications:
1. Under general anesthesia a. Assessment
Chest pain lasting more than 20 min, unrelieved by nitroglycerine
2. Median sternotomy and connected to cardiopulmonary bypass (CPB) machine ✓ Symptom must be evaluated with regard to time, duration, and the factors
ST-segment elevation in at least 2 leads that face the same area of the
3. Blood vessel is grafted, bypassing the obstruction that precipitate the symptom and relieve it; compare with previous
heart
4. CPB is discontinued symptoms
Less than 6 hours from onset of pain
5. Chest tubes and epicardial pacing wires are placed B. Nursing Diagnoses
THROMBOLYTICS: 6. Incision is closed ✓ Acute pain related to increased myocardial oxygen demand and decreased
7. Admitted to critical care unit myocardial oxygen supply
Absolute Contraindications:
✓ Risk for decreased cardiac tissue perfusion related to reduced coronary
▪ Active bleeding blood flow
▪ Known bleeding disorder ✓ Risk for imbalanced fluid volume
▪ History of hemorrhagic stroke ✓ Risk for ineffective peripheral tissue perfusion related to decreased cardiac
▪ History of intracranial vessel malformation output from left ventricular dysfunction
▪ Recent major surgery or trauma ✓ Anxiety related to cardiac event and possible death
▪ Uncontrolled hypertension ✓ Deficient knowledge about post-ACS self-care
▪ Pregnancy C. Planning
1. Relief of pain or ischemic S/S
Agents: 2. Prevention of myocardial damage
▪ alteplase (Activase) 3. Maintenance of effective respiratory function
▪ reteplase (Retavase) 4. Maintenance or attainment of adequate tissue perfusion
▪ tenecteplase (TNKase) 5. Reduced anxiety
6. Adherence to the self-care program
Nursing Considerations: 7. Early recognition of complications
▪ Minimize skin punctures D. Interventions
▪ Avoid IM injections 1. Relieve pain (primary focus)
▪ Draw blood specimens when starting the IV line ✓ Administer aspirin (S/E: epigastric distress & GI bleeding), beta-blocker,
▪ Start IV lines before thrombolytic therapy NTG, heparin
▪ Avoid continual use of noninvasive blood pressure cuff ✓ Administer morphine, oxygen via nasal cannula @ 2-4 LPM to maintain
▪ Monitor: acute dysrhythmias and hypotension O2 sat of 96%-100%
▪ Monitor for reperfusion: resolution of angina or acute ST-segment changes ✓ Physical rest with head and torso elevated
▪ Check for bleeding: 2. Improve respiratory function
✓ Encourage deep breathing and change position frequently
→ Decreased Hct and Hgb
3. Promote adequate tissue perfusion
→ Decreased BP
✓ Bed or chair rest during the initial phase until pt is pain-free and
→ Increased HR
hemodynamically stable
→ Oozing or bulging at invasive procedure sites
✓ Check skin temperature and pulses
→ Back pain
→ Muscle weakness 4. Reduce anxiety
→ Changes in level of consciousness
✓ Develop a trusting and caring relationship
→ Headache ✓ Provide information
→ Major bleeding: Off-Pump Coronary Artery Bypass Graft (OPCAB) ✓ Ensure a quiet environment
˗ discontinue thrombolytic therapy and anticoagulants ✓ Prevent interruptions in sleep
▪ Standard median sternotomy incision without CPB
˗ Apply direct pressure ✓ Use a caring & appropriate touch
▪ Beta-adrenergic blocker - used to slow the HR
˗ Notify primary provider ✓ Teach relaxation techniques
▪ A myocardial stabilization device is used to hold the site still for anastomosis of
→ Minor bleeding: ✓ Provide spiritual support
the bypass graft into the coronary artery while the heart continues to beat
˗ Apply direct pressure if accessible and appropriate ✓ Encourage to share concerns and fears
˗ Continue to monitor ✓ Convey acceptance
C. Coronary Artery Bypass Graft ✓ Music therapy, pet therapy
- A surgical procedure in which a blood vessel is grafted to an occluded
coronary artery so that blood can flow beyond the occlusion
 5. Diet: small easily digested meals (acute phase)
6. Monitor and manage potential complications
✓ Monitor changes in cardiac rate and rhythm, heart sounds, BP,
chest pain, respiratory status, urinary output, skin color,
temperature, sensorium, ECG changes, and lab values
7. Promoting home and community-based care
✓ Identify pt’s priorities
✓ Provide education about heart-healthy living
✓ Facilitate involvement in cardiac rehabilitation

CARDIAC REHABILITATION:

- Targets risk reduction by means of education, individual & group support &
physical activity
- Goals: To extend life & to improve quality of life.
- Phase I – begins with the diagnosis of atherosclerosis
→ Encourage physical activity
→ Client and family education
→ Provide counseling
- Phase II – from discharge until 4-6 weeks or up to 6 months
→ Supervised, often ECG-monitored exercise training
→ Support and guidance related to adherence to treatment program,
lifestyle modification
→ Outpatient cardiac rehabilitation program
˗ Phase III – focuses on maintaining cardiovascular stability and long-term
conditioning
→ Patient is already self-directed
E. Evaluation
✓ Relief of angina
✓ No signs or respiratory difficulties
✓ Adequate tissue perfusion
✓ Decreased anxiety
✓ Adherence to a self-care program
✓ Absence of complications
 #4 CARDIAC RHYTHM DISORDERS • 3 physiologic characteristics of nodal cells and Purkinje cells:
a. Automaticity – ability to initiate an electrical impulse
REVIEW OF THE PHYSIOLOGY OF THE HEART
b. Excitability – ability to respond to an electrical impulse
• Cardiac conduction system: generates and transmits electrical impulses that c. Conductivity – ability to transmit an electrical impulse from one cell to
stimulate contraction of the myocardium another
• Pacemakers of the heart
CARDIAC ACTION POTENTIAL:
a. Sinoatrial node
▪ primary pacemaker • Depolarization: electrical activation of a cell caused by the influx of sodium
▪ inherent firing rate (resting) = 60 – 100 bpm into the cell while potassium exits the cell (electrical stimulation)
b. Atrioventricular node • Systole: mechanical contraction
▪ Secondary pacemaker • Repolarization: return of the cell to resting state, caused by reentry of
▪ firing rate = 40 – 60 bpm potassium into the cell while sodium exits the cell
• Sodium – rapidly enters cell (atrial & ventricular myocytes) through sodium
fast channels
• Calcium – enters cell (cells of the SA & AV node) through slow channels

OBTAINING AN ECG:

• ELECTROCARDIOGRAPHY – the study of records of electrical activity

generated by the heart muscle
• ECG:
- a graphic representation of the electrical currents
- allows viewing of electrical conduction
- reflects waveform on screen/ paper which represents each phase of the
cardiac cycle
• Electrodes are attached to cable wires, which are connected to one of the
following:
a. ECG machine
b. Cardiac monitor
c. Telemetry
d. Holter monitor

WHAT IS A LEAD?

˗ an imaginary line that serves as a reference from which the electrical

activity is viewed
˗ STANDARD ECG: 12 LEADS
▪ Leads I, II, III
▪ Leads aVR, aVL, aVF
▪ Precordial Leads: V1, V2, V3, V4, V5, V6
▪ Others: 15-Lead ECG, 18-Lead ECG
▪ Most commonly used for continuous monitoring: Lead II and V1
PLACEMENT OF ELECTRODES FOR A STANDARD 12-LEAD ECG:
- 6 chest leads, 4 limb leads
a. Limb electrodes (4) – provides 1st 6 leads: I, II, III, aVR, aVL, AVF
b. Chest electrodes (6)
▪ V1 – 4 th ICS, Right sternal border
▪ V2 – 4 th ICS Left sternal border
▪ V3 – diagonally between V2 and V4
▪ V4 – 5 th ICS Left midclavicular line
▪ V5 – same level as V4, anterior axillary line
▪ V6 – same level as V4, V5, midaxillary line
NURSING CONSIDERATIONS (ECG):
• Electrodes are placed on dry, non-bony areas and in areas without significant
movement
• Connect electrodes to lead wires before placing them on the chest
• Peel the backing off the electrode
• Check skin for irritation (changed q 24-48 hrs)
• Don’t use adipose fats as landmarks
FOR A STANDARD 12-LEAD ECG:
• 6 chest leads,4 limb leads
• ECG waveforms are printed on graph paper:
▪ Horizontal axis –time and rate
▪ Vertical axis – amplitude or voltage
• Positive deflection
• Negative deflection
• ECG waveforms, complexes:
▪ P wave- represents atrial depolarization
mm in height
0.11 sec in duration
▪ QRS complex – represents ventricular depolarization
Less than 0.12 sec in duration
▪ T wave – represents ventricular repolarization (simultaneous with atrial
▪ PR interval (from beginning of P wave to the beginning of QRS complex)–
repolarization but is not visible because it occurs at the same time as the
the time needed for sinus node stimulation, atrial depolarization, and
QRS)
conduction through AV node before ventricular depolarization
▪ U wave – thought to represent repolarization of Purkinje fibers
0.12 – 0.20 sec in duration
Seen in patients with hypokalemia, HPN, or heart disease
▪ ST segment (from the QRS complex to the beginning of T wave)–
represents early ventricular repolarization
Normally isoelectric (when it is above or below the isoelectric line, a
sign of cardiac ischemia)
▪ QT interval (beginning of QRS complex to end of T wave) – represents the
total time for ventricular depolarization and repolarization
0.32 – 0.40 sec in duration
If prolonged, pt may be at risk for TORSADES DE POINTES (lethal)
 • sinus rhythm: electrical activity of the heart initiated by the SA node TYPES:
• normal sinus rhythm – electrical impulse starts at a regular rate and rhythm
A. SINUS NODE DYSRHYTHMIAS
in the SA
node TYPES:

NORMAL SINUS RHYTHM: a. Sinus Bradycardia (<60 bpm, regular rhythm)

• Ventricular & atrial rate: 60 to 100 (adult)
• Ventricular rate & rhythm: Regular
• QRS shape & duration: Usually normal but may be regularly normal
• P wave: Normal & consistent shape, always in front of the QRS
• PR interval: Consistent interval between 0.12 to 0.20 sec
• P:QRS ratio: 1:1
▪ Parasympathetic nervous system (vagal stimulation) causes automaticity of
the SA node to be depressed
▪ Causes: lower metabolic needs, vagal stimulation, medications, idiopathic
sinus node dysfunction, increased ICP, CAD, MI, hypoxemia, acute altered
mental status, HF
▪ DOC: atropine sulfate 0.5 mg IV bolus q 3-5 min. to a max total dose of 3
mg

Normal Sinus Rhythm Sinus Bradycardia

Ventricular & Atrial Rate 60 to 100 bpm Less than 60 bpm
Ventricular & Atrial Regular Regular
Rhythm
QRS Shape & Duration Usually normal, but may Usually normal, but may c. Sinus arrhythmia
be regularly abnormal be regularly abnormal ▪ Normal HR but irregular rhythm
P Wave Normal & consistent Normal & consistent ▪ sinus node creates an impulse at an irregular rhythm
shape; always in from of shape; always in from of ▪ Does not cause any significant hemodynamic effect and usually is not
the QRS the QRS treated
CARDIAC DYSRHYTHMIAS: PR Interval Consistent interval Consistent interval ▪ Cause: Heart disease, valvular disease (rare)
between 0.12 and 0.20 between 0.12 and 0.20 Normal Sinus Rhythm Sinus Bradycardia
• Dysrhythmias: disorders of the formation or conduction of the electrical
seconds seconds Ventricular & Atrial Rate 60 to 100 bpm 60 to 100 bpm
impulse within the heart, altering the heart rate, heart rhythm, or both and
P: QRS Ratio 1:1 1:1 Ventricular & Atrial Regular Irregular
potentially causing altered blood flow.
• Leads to decreased cardiac output Rhythm
• Most serious complication: SUDDEN CARDIAC DEATH b. Sinus tachycardia (100-120 bpm, regular rhythm) QRS Shape & Duration Usually normal, but may Usually normal, but may
▪ sinus node creates an impulse at a faster-than-normal rate be regularly abnormal be regularly abnormal
• Named according to the site of origin of the impulse and the mechanism of
▪ Causes: physiologic or psychological stress, medications that stimulate the P Wave Normal & consistent Normal & consistent
formation or conduction involved
sympathetic response, autonomic dysfunction shape; always in from of shape; always in from of
ETIOLOGY: the QRS the QRS
MANAGEMENT: PR Interval Consistent interval Consistent interval
• Increased sympathetic stimulation – exercise, anxiety, fever, administration
• Treat the underlying cause between 0.12 and 0.20 between 0.12 and 0.20
of catecholamines
seconds seconds
• If persistent & causing hemodynamic instability: Synchronized cardioversion
P: QRS Ratio 1:1 1:1
• Vagal maneuvers (carotid sinus massage, gagging, bearing down against a
closed glottis, forceful & sustained coughing, applying a cold stimulus to the
face)
• adenosisne (Adenocard) - for monomorphic QRS tachycardia
• procainamide (Pronestyl), amiodarone, sotalol (Betapace) - for wide QRS
tachycardia

Normal Sinus Rhythm Sinus Tachycardia

Ventricular & Atrial Rate 60 to 100 bpm 100 to 120 bpm
Ventricular & Atrial Regular Regular
Rhythm
QRS Shape & Duration Usually normal, but may Usually normal, but may
be regularly abnormal be regularly abnormal
P Wave Normal & consistent Normal & consistent
shape; always in from of shape; always in from of
the QRS the QRS
PR Interval Consistent interval Consistent interval
between 0.12 and 0.20 between 0.12 and 0.20
seconds seconds
P: QRS Ratio 1:1 1:1
 B. ATRIAL DYSRHYTHMIAS Normal Sinus Rhythm Atrial Fibrillation PHARMACOLOGIC CARDIOVERSION:
a. Premature Atrial Complex Ventricular & Atrial Rate 60 to 100 bpm Atrial rate: 300 - 600 bpm;
• Flecainide (Tambocor), amiodarone (w/in 7 days)
• Ectopic focus within one of the atria fires prematurely ventricular rate: 120 - 200
• Normal phenomenon in some individuals, “my heart skipped a beat,” may be bpm ELECTRICAL CARDIOVERSION:
caused by emotional disturbances, fatigue, tobacco, caffeine, anxiety, Ventricular & Atrial Regular Highly irregular
hypokalemia, hypermetabolic states or atrial injury, ischemia or infarction Rhythm • Hemodynamically unstable AFib (acute alteration in mental status, chest
discomfort, hypotension) and not responsive to medications
• Often seen with sinus tachycardia QRS Shape & Duration Usually normal, but may Usually normal, but may
c. Atrial Flutter (ventricular rate 75-150 bpm, usually regular)
be regularly abnormal be regularly abnormal
Normal Sinus Rhythm Premature Atrial
P Wave Normal & consistent No discernible P waves, • Occurs due to conduction defect in the atrium; atrial rate = 250 -450 per minute
Complex but is regular
shape; always in from of irregular undulating waves
Ventricular & Atrial Rate 60 to 100 bpm Depends on the • S/S: chest pain, shortness of breath, low BP
the QRS that vary in amplitude &
underlying rhythm (i.e.
shape (fibrillatory or f Normal Sinus Rhythm Atrial Flutter
sinus tachycardia)
waves) Ventricular & Atrial Rate 60 to 100 bpm Atrial rate: 250 - 400 bpm
Ventricular & Atrial Regular Irregular due to early P
PR Interval Consistent interval Cannot be measured Ventricular rate: 75 - 150
Rhythm waves
between 0.12 and 0.20 bpm
QRS Shape & Duration Usually normal, but may The QRS that follows the seconds
be regularly abnormal early P wave is usually Ventricular & Atrial Regular Atrial rhythm: Regular
P: QRS Ratio 1:1 Many:1 Rhythm Ventricular rhythm: usually
normal, but it may be
abnormal regular but may be
P Wave Normal & consistent An early & different P irregular
shape; always in from of wave or may be hidden in QRS Shape & Duration Usually normal, but may Usually normal (may be
the QRS the T wave; other P waves be regularly abnormal abnormal or absent)
are consistent P Wave Normal & consistent Saw-toothed shape (F
PR Interval Consistent interval The early P wave has a shape; always in from of waves)
between 0.12 and 0.20 shorter-than-normal PR the QRS
seconds interval but still within 0.12 PR Interval Consistent interval Multiple F waves may
to 0.20 seconds between 0.12 and 0.20 take it difficult to
P: QRS Ratio 1:1 Usually 1:1 seconds determine the PR interval
P: QRS Ratio 1:1 2:1, 3:1, or 4:1

• < 6 PACs per minute – no treatment necessary
• > 6 PACs per minute – indicate worsening of disease and onset of more
serious dysrhythmias (atrial fibrillation)
• Treatment: identify and treat the cause
b. Atrial Fibrillation (ventricular rate 120 – 200bpm, highly irregular)
• Atrial rate: 300 – 600 bpm
• A rapid, disorganized, and uncoordinated twitching of atrial musculature which
affects ventricular rate & rhythm as well
TO CONTROL THE HEART RATE:
TO CONVERT THE HEART RHYTHM OR PREVENT ATRIAL FIBRILLATION:
• Associated with: advanced age, valvular heart disease, CAD, HPN, heart
failure, DM, hyperthyroidism, congenital disorder of the heart, alcohol ingestion
• IMPORTANT CONSIDERATION: High risk of STROKE & premature death
due to possible clot formation 2⁰ erratic atrial contraction
• S/S: some are asymptomatic but others have:
▪ irregular palpitations
▪ S/S of HF (shortness of breath, fatigue, exercise intolerance, malaise)
▪ may cause: mitral valve dysfunction, mitral regurgitation, intraventricular
conduction delays
▪ pulse deficit
• MEDICAL MANAGEMENT:
Many AF convert to normal sinus w/in 24 - 48 hrs w/o treatment
• Low stroke risk - no antithrombotic therapy; may be placed on aspirin therapy • Vagal maneuvers
at 75 to 325 mg daily • Adenosine - to terminate the tachycardia
• Moderate risk for stroke - warfarin (Coumadin); direct-acting oral • Antithrombotic therapy
anticoagulant or Factor Xa inhibitor e.g. dabigatran (Pradaxal), rivaroxaban • Electrical cardioversion
(Xareltol), apixaban (Eliquis), edoxaban (Savaysa)
C. VENTRICULAR DYSRHYTHMIAS
• Beta-blockers (class II) - acebutolol (Sectral), propranolol (Inderal, InnoPran a. Premature Ventricular Complex (PVC) (depends on
XL) underlying rhythm, irregular)
• Non-dihydropyridine calcium channel blocker - verapamil (Isoptin), • An impulse that starts in a ventricle and is conducted through the ventricles
diltiazem (Cardizem) before the next normal sinus impulse.
• Causes: cardiac ischemia/ infarction, increased workload on the heart, digitalis
toxicity, hypoxia, acidosis, electrolyte imbalances
• For AFib lasting 48 hrs or longer - anticoagulation before attempts to restore • “My heart skipped a beat.”
sinus rhythm (pharmacological or electrical cardioversion)
 Normal Sinus Rhythm Premature Ventricular PR Interval Consistent interval Very irregular, if P waves • RAPIDLY FATAL & LIFE-THREATENING! cardiac death is IMMINENT if not
Complex between 0.12 and 0.20 are seen treated w/in 3-5 min
Ventricular & Atrial Rate 60 to 100 bpm Depends on the seconds • Causes: untreated VT, electrical shock, valvular heart disease; Brugada
underlying rhythm (e.g. P: QRS Ratio 1:1 Difficult to determine syndrome (pt w/ a structurally normal heart, few risk factors for CAD & family
sinus rhythm) hx of sudden cardiac death)
Ventricular & Atrial Regular Irregular (RR interval is
Normal Sinus Rhythm Ventricular Fibrillation
Rhythm shorter than others) PP
Ventricular & Atrial Rate 60 to 100 bpm Ventricular rate: Greater
interval may be regular
than 300 bpm
QRS Shape & Duration Usually normal, but may Duration: 0.12 seconds or
be regularly abnormal longer; shape is bizarre Ventricular & Atrial Regular Ventricular rhythm:
and abnormal Rhythm Extremely irregular,
without a specific pattern
P Wave Normal & consistent Visibility of P wave
QRS Shape & Duration Usually normal, but may Irregular, undulating
shape; always in from of depends on the timing of
the QRS the PVC; may be absent be regularly abnormal waves with changing
or in front of QRS; shape amplitudes; no
may be different recognizable QRS
complexes
PR Interval Consistent interval If the P wave is in front of
P Wave Normal & consistent Visibility of P wave
between 0.12 and 0.20 the QRS, the PR interval
seconds is less than 0.12 seconds shape; always in from of depends on the timing of
the QRS the PVC; may be absent
P: QRS Ratio 1:1 0:1; 1:1
or in front of QRS; shape
Considered an EMERGENCY! may be different
CAUSES OF PVC: PR Interval Consistent interval If the P wave is in front of
• patient is usually unresponsive and pulseless-cardiac arrest between 0.12 and 0.20 the QRS, the PR interval
✓ Cardiac ischemia or infarction
seconds is less than 0.12 seconds
✓ Increase cardiac workload (HF) MANAGEMENT: Factors to determine initial treatment:
P: QRS Ratio 1:1 0:1; 1:1
✓ Digitalis toxicity
• Identifying the rhythm as monomorphic or polymorphic
✓ Hypoxia, acidosis and hypokalemia
• Existence if a prolonged QT interval before the initiation of VT
TYPES: • Any comorbidities
• Ascertaining the heart function
▪ Bigeminy – every other complex is a PVC
▪ Trigeminy – every third complex is a PVC • If stable: Continue assessment (ECG)
▪ Quadrigeminy – every fourth complex is a PVC • Monomorphic stable VT (no MI or severe HF)
▪ Procainamide
▪ Sotalol
• IV amiodarone (medication of choice) – if with impaired cardiac function or MI
• Lidocaine - most commonly used for immediate, short-term therapy
• Cardioversion (treatment of choice) – monophasic, symptomatic VT
• Defibrillation (treatment of choice) – pulseless VT
• Long-term management: – <35% ejection fraction – implantable cardioverter
defibrillator (ICD)
• Torsades de Pointes: a polymorphic VT preceded by a prolonged QT interval
▪ Requires immediate treatment – Correct electrolyte imbalance
IV magnesium
IV isoproterenol (Isuprel)
Pacing (if with bradycardia)

MANAGEMENT OF PVC:

• Usually not serious

• If more frequent: amiodarone or sotalol
b. Ventricular Tachycardia (100 -200 bpm, regular)
• 3 or more PVCs in a row, occurring at a rate exceeding 100 bpm
• Usually associated with CAD and MI, may precede Vfib

Normal Sinus Rhythm Ventricular Tachycardia

Ventricular & Atrial Rate 60 to 100 bpm Ventricular rate: 100-200
bpm Atrial rate: depends
on the underlying rhythm
Ventricular & Atrial Regular Usually regular
Rhythm
c. Ventricular Fibrillation (greater than 300 bpm, extremely
QRS Shape & Duration Usually normal, but may 0.12 seconds or more;
irregular)
be regularly abnormal bizarre, abnormal shape
• A rapid, disorganized ventricular rhythm that causes ineffective quivering of the
P Wave Normal & consistent Very difficult to detect so
ventricles characterized by absence of audible heartbeat, a palpable pulse and
shape; always in from of the atrial rate and rhythm
respirations
the QRS may be indeterminable
• No atrial activity seen on ECG
MANAGEMENT: • Same management with asystole and pulseless electrical activity (PEA) if in P: QRS Ratio 1:1 1:1
cardiac arrest
• Treatment of choice: bystander CPR till defibrillation is available + activation
• Same with bradycardia if not in arrest
of emergency services
• Identify the underlying cause
• For refractory Vfib - amiodarone and epinephrine may facilitate the return of
• IV epinephrine
spontaneous pulse after defibrillation
• Atropine
d. Idioventricular Rhythm
• Vasopressor medications
• Ventricular escape rhythm
• Emergency transcutaneous pacing
• Occurs when the impulse starts in the conduction system below the AV node
e. Ventricular Asystole (flatline)
• The purkinje fibers automatically discharge an impulse
• Absent QRS complexes in 2 different leads
• If not caused by an AV block, it has the following characteristics: (next slide)
• No heartbeat, no palpable pulse, no respiration
• Results to loss of consciousness and symptoms of reduced cardiac output
• Fatal without immediate treatment
• May cause no symptoms of reduced CO in some

Normal Sinus Rhythm Idioventricular Rhythm

Ventricular & Atrial Rate 60 to 100 bpm
Ventricular & Atrial Regular
Rhythm
QRS Shape & Duration Usually normal, but may
be regularly abnormal
P Wave Normal & consistent
shape; always in from of
the QRS
PR Interval Consistent interval
between 0.12 and 0.20
seconds
P: QRS Ratio 1:1
Ventricular rate: 20-40
bpm If the rate exceeds
40 bpm, the rhythm is
known as accelerated
idioventricular rhythm
Regular
Bizarre, abnormal shape;
duration is 0.12 seconds
or more
Visibility of P wave
depends on the timing of
the PVC; may be absent
or in front of QRS; shape B. Second-Degree Atrioventricular Block, Type 1 (Mobitz I, Wenckebach)
may be different ▪ Occurs when there is a repeating pattern in which all but one of a series of
If the P wave is in front of atrial impulses are conducted through the AV node into the ventricles
the QRS, the PR interval ▪ Each atrial impulse takes longer time for conduction than the one before,
is less than 0.12 seconds until one impulse is fully blocked
0:1; 1:1 Normal Sinus Rhythm Second-Degree
Atrioventricular Block,
MANAGEMENT: Type I (Mobitz I,
• Treatment: high-quality CPR with minimal interruptions Wenckebach)
• Identify and treat underlying cause Hs and Ts: hypoxia, hypovolemia, Ventricular & Atrial Rate 60 to 100 bpm Depends on underlying
hydrogen-ion (acid-base imbalance), hypo-or hyperglycemia, hypo- or rhythm but the ventricular
hyperkalemia, hyperthermia, trauma, toxins, tamponade (cardiac), tension rate is lower than the atrial
rate
pneumothorax, or thrombus (coronary or pulmonary)
Ventricular & Atrial Regular PP interval: Regular if
CONDUCTION ABNORMALITIES: Rhythm normal sinus rhythm RR
interval: Reflects a pattern
• AV blocks occur when the conduction of the impulse through the AV nodal or
of change
Bundle of His area is decreased or stopped
QRS Shape & Duration Usually normal, but may Usually normal but may
TYPES OF CONDUCTION ABNORMALITIES: be regularly abnormal be abnormal
P Wave Normal & consistent In front of the QRS
A. First-Degree Atrioventricular Block
shape; always in from of complex; shape depends
▪ Occurs when all the atrial impulses are conducted through the AV node into
the QRS on underlying rhythm
the ventricles at a rate slower than normal
PR Interval Consistent interval Becomes longer with each
Normal Sinus Rhythm First-Degree between 0.12 and 0.20 succeeding ECG complex
Atrioventricular Block seconds until there is a P wave not
Ventricular & Atrial Rate 60 to 100 bpm Depends on underlying followed by a QRS
rhythm P: QRS Ratio 1:1 3:2, 4:3, 5:4, and so forth
Ventricular & Atrial Regular Depends on underlying
Rhythm rhythm
QRS Shape & Duration Usually normal, but may Usually normal but may
be regularly abnormal be abnormal
P Wave Normal & consistent In front of the QRS
shape; always in from of complex, shows sinus
the QRS rhythm, regular shape
PR Interval Consistent interval Greater than 0.20
between 0.12 and 0.20 seconds, PR interval
seconds measurement is constant
 C. Second-Degree Atrioventricular Block, Type II (Mobitz II)
▪ Occurs when only some of the atrial impulses are conducted through the
AV node into the ventricles
Normal Sinus Rhythm Second-Degree
Atrioventricular Block,
Type II (Mobitz II)
Ventricular & Atrial Rate 60 to 100 bpm Depends on underlying
rhythm but the ventricular
rate is lower than the atrial
rate
Ventricular & Atrial Regular PP interval: Regular if
Rhythm normal sinus rhythm RR
interval: Usually regular
but may be irregular
depending on the P;QRS
ratio
QRS Shape & Duration Usually normal, but may Usually abnormal but may
be regularly abnormal be normal
P Wave Normal & consistent In front of the QRS
shape; always in from of complex; shape depends
the QRS on underlying rhythm
PR Interval Consistent interval Constant for those P
between 0.12 and 0.20 waves just before QRS
seconds complexes
P: QRS Ratio 1:1 2:1, 3:1, 4:1, 5:1 and so
forth
D. Third-Degree Atrioventricular Block (Complete block)
▪ Occurs when no atrial impulse is conducted through the AV node into the
ventricles
Normal Sinus Rhythm Third-Degree
Atrioventricular Block
(Complete Block)
Ventricular & Atrial Rate 60 to 100 bpm Depends on the escape
rhythm (idionodal or
idioventricular) and
underlying atrial rhythm,
but the ventricular rate is
lower than the atrial rate
Ventricular & Atrial Regular PP interval: Regular RR
Rhythm interval: Regular But PP
interval is not equal to RR
interval
QRS Shape & Duration Usually normal, but may Depends on the escape
be regularly abnormal rhythm; with junctional
rhythm, QRS shape and
duration are usually
normal; with
idioventricular rhythm,
duration and share are
usually abnormal
P Wave Normal & consistent Depends on the
shape; always in from of underlying rhythm
the QRS
PR Interval Consistent interval Very irregular
between 0.12 and 0.20
seconds
P: QRS Ratio 1:1 More P waves than QRS
complexes
CARDIAC DYSRHYTHMIAS
COMPLICATIONS:
• Cardiac arrest
• Heart failure
• Thromboembolic event (esp. with atrial fibrillation)
MEDICAL MANAGEMENT:
A. ANTIARRHYTHMIC MEDICATIONS:
a. I – Na+ Channel Blockers
▪ Quinidine (Quinidex)
▪ Procainamide (Procar S)
▪ Lidocaine (Xylocaine)
b. II – Beta-Adrenergic Blocking Agents (BABAs)
▪ Atenolol (Tenormin) c
c. III – K= Channel Blockers
▪ Amiodarone (Cordarone)
d. IV – Ca+ Channel Blockers
▪ Verapamil (Isoptin)
▪ Diltiazem (Cardizem)
B. VAGAL MANEUVERS
• induce vagal stimulation of the cardiac conduction system; used to
terminate supraventricular tachydysrhythmias
1. Carotid Massage
→ Physician instructs client to turn the head away from the side to be
massaged
→ The carotid artery is massaged for 6-8 sec until there is a change in
the cardiac rhythm
→ Observe cardiac monitor
→ Record an ECG rhythm strip before, during & after the procedure
→ Have a defibrillator & resuscitative equipment available
→ Monitor VS, cardiac rhythm & LOC after the procedure
2. Valsalva maneuver
▪ Physician instructs client to bear down or induce a gag reflex in the
client, both of which stimulate the vagal reflex
▪ Monitor HR, rhythm & BP
▪ Observe the cardiac monitor
▪ Record an ECG rhythm strip before, during & after the procedure
▪ Have a defibrillator & resuscitative equipment available
▪ Provide an emesis basin if the gag reflex is stimulated, and initiate
precautions to prevent aspiration
C. CARDIOVERSION: electrical current administered in synchrony with the pt’s
own QRS complex to stop a dysrhythmia
• An elective procedure done by the physician
• A lower amount of energy is used than with defibrillation
 • Cardioversion is synchronized to the client’s R wave to avoid discharging
the shock during the vulnerable period (T wave)
• If the cardioverter were not synchronized, it would discharge on the T wave
and cause VF
✓ Ensure that no one is touching the client, to avoid motion artifact during
rhythm analysis
✓ Place the electrode paddles in the correct position on the client’s chest
✓ Press the analyser button to identify the rhythm, which may take 20
sec; the machine will advise if shock is necessary
✓ Shocks are recommended for pulseless VF only

• Pacemaker Therapy: an electronic device that provides electrical stimuli to

the heart muscle; may be temporary or permanent
• Implantable Cardioverter Defibrillator: a device that detects and terminates
life-threatening episodes of tachycardia or fibrillation

IMPLEMENTATION:

• Pre-procedure:
✓ Obtain consent
✓ Administer sedation as prescribed
✓ Hold Digoxin (Lanoxin) 48 hours pre-procedure to prevent post-
cardioversion ventricular irritability NURSING MANAGEMENT:
• During: I. Assessment
✓ Ensure that the skin is clean & dry in the area where the electrode paddles ✓ Possible causes of the dysrhythmia and contributing factors
will be placed ✓ Effects on the heart’s ability to pump
✓ Stop the O2 during the procedure to avoid hazard of fire ✓ History
✓ Be sure that no one is touching the bed or the client when delivering the ✓ Psychosocial assessment
countershock ✓ Physical assessment
• Post-procedure: II. Diagnoses
✓ Maintain airway patency ✓ Decreased cardiac output
✓ Administer O2 as prescribed ✓ Anxiety related to fear of the unknown
✓ Assess VS ✓ Deficient knowledge about the dysrhythmia and its treatment
✓ Assess LOC III. Planning
✓ Monitor for cardiac rhythm ✓ Eliminate or decrease occurrence of dysrhythmia to maintain cardiac
✓ Monitor for indications of successful response: conversion to sinus rhythm, output
strong peripheral pulses and an adequate BP ✓ Minimize anxiety
D. DEFIBRILLATION ✓ Acquire knowledge about dysrhythmia and its treatment
• electrical current administered to stop a dysrhythmia, not synchronized IV. Interventions
with the pt’s QRS complex 1. Monitoring and managing the dysrhythmia
• 3 rapid consecutive shocks are delivered with the first at an energy of 200 ✓ Administer antiarrhythmic medications
joules ✓ Administer a 6-minute walk test
• If unsuccessful, the shock is repeated to 200-300 joules 2. Minimizing anxiety
• 3rd: 360 joules ✓ Maintain a calm, reassuring attitude
✓ Emphasize successes in treatment to the pt
IMPLEMENTATION:
✓ Help pt develop a system to identify possible causative,
✓ Stop the O2 during the procedure to avoid hazard of fire influencing, and alleviating factors
✓ Be sure that no one is touching the bed or the client when delivering the 3. Promoting home and community-based care
countershock ✓ Importance of maintaining therapeutic serum levels of
✓ Use of paddle electrodes: antiarrhythmics
▪ Apply conductive pads ✓ Establish a plan of action to take in case of emergency
▪ One paddle: 3rd ICS R of sternum the other paddle: 5th ICS L midaxillary ✓ Teach about potential effects of the dysrhythmia and their s/s
line V. Evaluation
▪ Apply firm pressure with the paddles ✓ Maintains cardiac output
▪ Be sure that no one is touching the bed or the client when delivering the ✓ Experiences reduced anxiety
countershock ✓ Expresses understanding of the dysrhythmia and its treatment
E. AUTOMATIC EXTERNAL DEFIBRILLATOR (AED)
▪ Used by laypersons and emergency medical technicians to prehospital
cardiac arrest
✓ Place the client on a firm, dry surface
✓ Stop CPR
 #5 ASTHMA PEAK FLOW MONITORING:

• Reader’s Theater: Will, Age 9 In your notebook… • Measures the highest airflow during a forced expiration
- Note for significant data: • Daily monitoring: “personal best” is determined
→ Predisposing/ contributing factors ▪ Green zone: 80-100% of personal best
→ History ▪ Yellow zone: 60-80%
→ Manifestations ▪ Red zone: <60%
→ Management
• Validate your notes’ accuracy as the discussion is going on.

ASSESSMENT:

• Complete family, environmental, and occupational history

• Comorbid conditions

PREVENTION:

• Avoid causative agents: dust mites, roaches, pollens, molds

• Client education

MEDICAL MANAGEMENT:

• Pharmacologic therapy
1. quick-relief medications – short-acting
2. long-acting medications
• Common allergens: Seasonal: grass, tree, & weed pollens
• Route of choice: metered dose inhaler (pMDI) PHARMACOLOGIC THERAPY:
• Perennial allergens: Molds, Dust Mites, Animal Dander
METERED-DOSE INHALER: A. Quick-relief medications
• pressurized device containing an aerosolized powder of medication a. Short-acting beta2 -adrenergic agonist (SABA)
→ Medication of choice for relief of acute symptoms & prevention
of exercise-induced asthma
→ Relaxes smooth muscle
→ Ex: Albuterol (Ventolin); Levalbuterol (xopenex); Pirbuterol
(Maxair)
 b. Anticholinergics d. a return of ABG levels to normal limits
→ inhibit muscarinic cholinergic receptors and reduce intrinsic vagal e. O2 saturation greater than 95%
tone of the airway ✓ Assess frequently, observe RR & depth
→ For patients who cannot tolerate beta adrenergics agonists ✓ Assess: shortness of breath, pursed-lip breathing, nasal flaring, sternal and
→ Ex: ipratropium bromide [Atrovent] intercostal retractions, or prolonged expiratory phase
B. Long-acting: maintain control of persistent asthma ✓ Place on Fowler’s position – to facilitate maximum lung expansion
a. Corticosteroids ✓ O2 as ordered
→ Most potent & effective anti-inflammatory ✓ Monitor ABG and O2 saturation levels
→ Use spacer and rinse mouth to prevent oral thrush 3. Impaired Gas Exchange – related to trapped air in the alveoli and imbalance
→ Systemic form: to gain rapid control, manage severe asthma/ in O2 and CO2
exacerbations, prevent recurrence - Goal: Establish an adequate gas exchange as evidenced by:
b. Mast cell stabilizer a. decreased abnormal breath sounds
→ Ex: Cromolyn sodium (Intal) nedocromil (Tilade) b. ABG levels within normal limits
c. usual skin color
→ Mild-moderate anti-inflammatory agent
d. decreasing dry, non-productive cough B. Arterial Blood Gas Studies
→ Preventive treatment prior to exposure to exercise or known
✓ Assess lung sounds every hour (acute episodes) – to help evaluate if there - Assesses ability of lungs to provide adequate oxygen and remove carbon
allergen
is adequate gas exchange dioxide and the ability of the kidneys to reabsorb or excrete bicarbonate
→ C/I in acute asthma exacerbations
✓ Assess skin and mucous membranes for cyanosis ions to maintain normal body pH
c. Long-acting beta2 - adrenergic agonists
✓ Monitor pulse oximetry - pH
→ For long-term control of asthma symptoms (esp. occurring at night)
✓ O2 as ordered - PaO2
→ Effective for prevention of exercise-induced asthma
4. Anxiety - PaCO2
→ Ex: salmeterol (serevent) formoterol (Foradil) 5. Activity Intolerance - HCO3
d. Methylxanthines 6. Altered nutrition: Less than body requirements C. Pulse Oximetry
→ Ex: theophylline [Slo-bid, Theo-Dur] aminophylline 7. Sleep Pattern Disturbance - Continuous monitoring of the oxygen saturation of hemoglobin (SaO2),
→ Mild- moderate bronchodilators referred to as SpO2
→ For relief of night-time asthma symptoms - N = 95% - 100%
e. Leukotriene modifier (inhibitors) ONE-SENTENCE SUMMARY In your notebooks, write a single sentence that sums - Less than 85% - indicate that the tissues are not receiving enough oxygen
→ Dilate blood vessels and alter permeability up what should essentially be remembered about asthma. You have two (2) minutes - Unreliable in states of low perfusion, hypothermia, nail polish
→ Ex: montelukast (Singulair) zileuton (Zyflo) to do this.
f. Immunomodulators
→ Prevent binding of IgE to the receptors of basophils and mast cells
→ Ex: omalizumab (Xolair) A. Pulmonary Function Tests (PFT)
NURSING MANAGEMENT: - include measurements of lung volumes, ventilatory function, and the
mechanics of breathing, diffusion, and gas exchange
• Assessment - Spirometer – a volume-collecting device attached to a recorder that
→ Use calm approach demonstrates volume and time simultaneously
→ Assess for airway distress
→ History of allergic reactions to medications
→ Assess respiratory status: severity of symptoms, breath sounds, peak flow,
pulse oximetry, vital signs
→ Current medication use
→ Fluid status – insensible fluid loss is increased ➔dehydration
→ Ability to manage asthma & general adaptation
→ Presence of triggers

NURSING DIAGNOSES, OUTCOMES & INTERVENTIONS:

1. Ineffective Airway Clearance – lead to production of mucus and spasm of the

D. Cultures
airway
- Throat culture
- Goal: Establish an effective airway clearance as evidenced by: a.
- Nasal swab
decreased abnormal breath sounds b. decreasing dry, non-productive
E. Sputum studies
cough
- To assess for pathogenic organisms, assess for hypersensitivity states,
✓ Suctioning (for compromised airway)
immunosuppressive medications
✓ Assist in coughing effectively
- Early morning specimen – expectoration
✓ Encourage oral fluids – to thin secretions
✓ Chest physiotherapy
✓ Expectorants – mucolytics first as prescribed before giving
expectorants
✓ Frequent position changes
✓ Oral care every 2-4 hours – to remove the taste of secretions
2. Ineffective Breathing Pattern – related to airway spasm and edema
- Goal: Improved breathing patterns as evidenced by:
a. RR with normal limits
b. decreased dyspnea, less nasal flaring, and reduced use of
accessory muscles
c. decreased signs of anxiety
 #6 COPD (Chronic Obstructive Pulmonary Disease) COPD:

• Progressive chronic airflow limitation associated with abnormal inflammatory RISK FACTORS:
response that is not fully reversible.
➢ Cigarette smoking – smoking depresses the activity of the scavenger cells
• Includes diseases that cause airway obstruction.
and the respiratory tract’s cleansing mechanism
➢ Passive smoking – inhalation of smoke
➢ Prolonged and intense exposure to occupational dusts & chemicals, air
A. CHRONIC BRONCHITIS pollution
˗ Presence of cough and sputum production for at least 3 months in each of ➢ Host risk factor: Alpha 1 antitrypsin deficiency
2 consecutive years (smoke & environmental pollutants – damage alveoli - Enzyme inhibitor that protects the lung parenchyma from injury
(inflammation))
˗ Constant irritation→ increase in number of mucus secreting gland and CLINICAL MANIFESTATIONS/SIGNS & SYMPTOMS:
goblet cells, reduced ciliary function, more mucus produced
➢ Primary symptoms: chronic cough (may be intermittent, non-productive),
˗ Adjacent alveoli become damaged and fibrosed (scarred) → patient
sputum production, and dyspnea on exertion → dyspnea at rest
susceptible to respiratory infection (altered function of alveolar
➢ Weight loss: dyspnea interferes with eating, work of eating is energy depleting
macrophages)
➢ Use of accessory muscles for breathing
➢ Advanced emphysema: abdominal muscles also contract on inspiration

*Hypoxia – decreased O2 in the tissues

b. Centilobar (centroacinar)
→ Pathologic changes: mainly in the center of the secondary lobule
→ Produces hypoxemia (decreased O2 in blood), hypercapnia (increased
CO2), polycythemia (increased RBC) vera, & episodes of right-sided
heart failure
→ Central cyanosis (bluish discoloration of the lips), peripheral edema, &
respiratory failure *Peripheral cyanosis – bluish discoloration of the
extremities

B. EMPHYSEMA
˗ Abnormal distention of the airspaces and destruction of the walls of over-
distended alveoli (damage to the alveolar walls → the alveolar surface in direct
contact with pulmonary capillaries ill decrease)
˗ Increase in dead space (no gas exchange) & impaired oxygen diffusion *Dependent edema

˗ Complication: Right sided heart failure (cor pulmonale – “heart of the lungs”) *Distended neck
veins/jugular veins
˗ Types of Emphysema:
a. Panlobar (panacinar)
→ Destruction of the respiratory bronchiole, alveolar duct, &
alveoli
→ All air spaces within the lobule - inflamed (little inflammatory
disease)
→ Barrel chest, dyspnea on exertion (eventually leads to dyspnea
at rest), weight loss
→ Respiration becomes active & requires muscular effort
 ➢ ABG (Arterial Blood Gas)
- Respiratory acidosis, decrease in O2 saturation and PO2

ASSESSMENT:
➢ Chest X-ray
➢ Health history
➢ Physical assessment
- Nasal polyps: fleshy inflammations that grow on the inside of the nose or
in sinuses and mostly target young and middle-aged adults.
- Nasal polypectomy: removal of polyps in the nasal passages

DIAGNOSTIC:

➢ Spirometry
˗ Evaluate airflow obstruction
˗ Determined by the ratio of FEV1 (volume of air that the patient can forcibly
exhale in 1 second) to FVC (forced vital capacity)
➢ Bronchodilator reversibility testing – to determine maximum lung expansion
- Rule out diagnosis of asthma & to guide initial treatment

SIPORMETRY & BRONCHODILATORS: COMPLICATIONS:

RESULTS:
1 Spirometry ➢ Respiratory insufficiency & failure
*Improved after bronchodilator was given = ASTHMA ➢ Infection
2 Bronchodilator
No improvement after bronchodilators = COPD ➢ Pneumonia
3 Spirometry again
➢ Chronic atelectasis
➢ Pneumothorax – air inside the pleural cavity
➢ cor pulmonale – LSHF (left-sided heart failure)
MEDICAL MANAGEMENT: ➢ Lung Transplantation - Improving Breathing Patterns
- Alternative for definitive treatment of end-stage emphysema Diaphragmatic breathing
➢ Risk reduction
Pursed-lip breathing
- Smoking cessation PULMONARY REHABILITATION:

Challenges: nicotine-addictive, setting, depression, habit
1. Explain the risks of smoking
2. Set a quit date
3. Refer to support groups or smoking cessation programs
4. Follow-up 3-5 days after quit date (phone call, clinic visits)
5. Relapses: assess and analyze what happened
Pack Years: No. of packs consumed per day x no. of years the pt. has smokes
➢ Goals: Reduce symptoms, improve quality of life and increase physical and
emotional participation in everyday activities.
- For Grade II to IV COPD
- Minimum length: 6 weeks
- Programs:
Education (smoking cessation, physical reconditioning, nutritional
counseling, skills training, psychological support)

˗ Nicotine replacement – 1st line pharmacotherapy (gum, inhaler, lozenges, Packed Years: 2 packs per day x 5 years
nasal spray, transdermal patch, SL tablets) Packed Years: 10
˗ Bupropion SR (Wellbutrin)
ANTIDEPRESSANTS ➢ Improving Activity Tolerance
˗ nortriptyline (Aventyl)
➢ Enhancing Self-care strategies
˗ Clonidine (Catapress) – anti-hypertensive agent; side effects may limit use
NURSING MANAGEMENT: - Setting realistic goals
➢ Varenicline (Chantix) – nicotinic acetylcholine receptor partial agonist (may
- Avoiding temperature extremes
assist in smoking cessation) ➢ Patient Education
Heat increases body temp. → ↑se O 2 requirements
➢ Pharmacologic Therapy ➢ Breathing Exercises
Cold promote bronchospasm
- Bronchodilators: relieve bronchospasm & reduce airway obstruction - Diaphragmatic breathing: Goal: To use and strengthen the diaphragm
➢ Modifying Lifestyle
Metered-dose inhaler during breathing
➢ Enhancing Individual Coping Strategies
Classes: beta-adrenergic agonist, anticholinergic agents, & Place one hand on the abdomen and the other hand on the middle of
➢ Monitoring & Managing Potential Complications
methylxanthines the chest
˗ Corticosteroids Breathe in slowly and deeply through nose, letting the abdomen
˗ Other medications protrude as far as possible
Influenza vaccine: yearly Breathe out through pursed lips while tightening the abdominal muscles
Pneumococcal vaccine: every 5-7 years Press firmly inward and upward on the abdomen while breathing out.
- Pursed-lip breathing
➢ Activity Pacing
➢ Self-care activities
➢ Physical Conditioning
- Breathing exercises
- Treadmills
- Stationary bicycles
- Measured level walks
➢ Oxygen therapy
- Caution that smoking near O2 is dangerous!
➢ Nutritional Therapy
- Assess caloric needs and monitor weight
➢ Coping Measures

NURSING PROCESS:

➢ Assessment
- Health history
- Inspection and examination findings
➢ Diagnoses
- Impaired gas exchange related to ventilation-perfusion inequality
MANAGEMENT OF EXACERBATION: - Ineffective airway clearance related to bronchoconstriction, increased
mucus production, ineffective cough, bronchopulmonary infection
➢ Supplemental O2 therapy & rapid assessment: 1st line treatment - Ineffective breathing pattern related to shortness of breath, mucus,
➢ Short-acting bronchodilator + oral/IV corticosteroids bronchoconstriction
➢ OXYGEN THERAPY ➢ Planning and Goals
- Indicated for PaO 2 of 55 mm Hg or less. (80-100 mmHg) - Smoking cessation
- Goal: - Improve gas exchange, airway clearance, improve breathing pattern
Increase PaO2 to at least 60 mmHg ➢ Nursing Interventions
Increase SaO2 to at least 90% - Promoting Smoking Cessation
SURGICAL MANAGEMENT: - Improving Gas exchange
Monitor patient for dyspnea & hypoxemia
➢ Bullectomy (Bullae) Administer medications: bronchodilators & corticosteroids
- Surgical excision of bullous emphysema - Achieving Airway clearance
- Done thoracoscopically or via limited thoracotomy incision Directed coughing: controlled coughing
➢ Lung Volume Reduction Surgery - Chest physiotherapy w/ postural drainage, intermittent positive-pressure
- Removal of a portion of the diseased lung parenchyma breathing, increased fluid intake, bland aerosol mists
 #7 ACID BASE BALANCES & IMBALANCES ABG ANALYSIS AND INTERPRETATION

• ACIDS- “H+” ion donors - Steps:

- 2 Forms: 1. Classify pH whether normal, acidosis, alkalosis
a. Volatile- excreted as gas: CO2 + H2O ➔ H2CO3 (carbonic acid) ▪ Normal: 7.35-7.45
▪ e.g., PC02 (LUNGS) = 35-45 mmHg – - indicates CO2 levels in ▪ Normal but slightly acidic (7.36-7.39)
blood & reflects ventilation ▪ Normal but slightly alkaline (7.45-7.49)
b. Nonvolatile- excreted as body fluids (urine) ▪ < 7.35 – acidosis
▪ e.g., sulfuric acid, lactic acid, phosphoric acid ▪ >7.45 – alkalosis
2. Assess PCO2 (CO2 – acid), whether normal, acidosis, alkalosis
HYPOVENTILATING = increased PCO2 ▪ Normal: 35-45
HYPERVENTILATING = decreased PCO2 ▪ <35 mmHg – alkalosis
▪ >45 mmHg – acidosis
• BASES- “H+” ion acceptors – substances that bind with H+ when dissolved in 3. Assess HCO3 (CO3 – base), whether normal, acidosis, alkalosis
H2O ▪ Normal: 22-26
- E.g: ▪ <22 mEq/L – acidosis
a. Strong bases ▪ >26 mEq/L – alkalosis
▪ Na OH (sodium hydroxide) 4. Determine the primary problem (same interpretation)
▪ NH3 (ammonia) ▪ PCO2 → pH = RESPIRATORY DISORDER
b. Al OH (aluminum hydroxide) ▪ HCO3 → pH = METABOLIC DISORDER
c. HCO3 (bicarbonate) – KIDNEYS *Normal: HCO3 = 22-26 mEq/L 5. Determine the presence of compensation by checking the value not the
• pH - the negative logarithm of the H+ ion concentration same as the pH
*Normal: 7.35 – 7.45 (blood pH)
- Increased pH: Decreased H+ ions ▪ Partially compensated
- Decreased pH: Increased H+ ions Decreased: Acidic → PCO2/HCO3 opposite interpretation w/ pH
- expresses the acidity or alkalinity of a solution Increased: Alkaline → pH is ABNORMAL
▪ Fully compensated
• Plasma pH – an indicator of Hydrogen ion (H+) concentration maintained → PCO2/HCO3 opposite interpretation w/ pH
normal due to the body’s homeostatic mechanisms consist of: buffer systems, → pH is NORMAL
the kidneys (HCO3), and lungs (CO2). ▪ Uncompensated
- The greater the concentration, the more acidic the solution, and the lower → PCO2/HCO3 is NORMAL
the Ph → pH is NOT NORMAL
BUFFER SYSTEMS

- systems comprised of substances/ organs capable of binding (removing)

H+ ion from body fluids or releasing H+ quickly to prevent major changes in
pH
- Important regulator of pH
a. Chemical Buffers
▪ Bicarbonate-carbonic acid buffer – major extracellular buffer
system
→ HCO3 (bicarbonate) and H2CO3 (carbonic acid) combine w/
HCl = decrease the strength of potentially damaging acids &
bases
▪ Phosphate buffer system – increased amount of NaHCO3
(sodium bicarbonate) in the ECF making it more alkaline
▪ Protein buffer – Hgb – a major protein buffer w/c maintains pH in
the blood
b. Respiratory Buffers
▪ The lungs regulate blood levels of CO2
▪ CO2 = H2O = H2CO3 (carbonic acid)
▪ Increased H2CO3 ➔ decreased pH (more H+)
▪ 2nd line of defense; twice as effective but only temporary
c. Renal Buffer
▪ Kidney’s conserve circulating stores of HCO3 and to excrete H+
▪ Effective yet relatively slow (hours to days)
▪ Increase urinary excretion of H+ & conserving plasma
→ HCO3 ➔ if blood is too acidic
▪ Decrease urinary excretion of H+ & urinary excretion of
→ HCO3 ➔ if blood is too alkaline
 #8 BURNS CLASSIFICATION OF BURNS BY EXTENT OF INJURY:

BURN, INJURIES 1. MINOR BURN INJURY

▪ Second-degree burn of <15% total body surface area (TBSA) in adults or
• Approximately 1.1 million people require medical attention for burns every
<10% TBSA in children.
year, and about 4,500 persons die of burns and associated inhalation injuries
▪ Excludes all patients with electrical injury, inhalation injury, or concurrent
every year.
trauma and all poor-risk patients (e.g, extremes of age, intercurrent
• Incidence: any person, any time, any place, across socioeconomic groups disease)
• Most burns occur in the home, can occur in workplace (65 y.0) 2. MODERATE, UNCOMPLICATED BURN INJURY
• Young children and the elderly are at high risk for burn injuries. ▪ Second-degree burns of 15-25% TBSA in adults or 10-20% in children
• Nurses must play an active role in the prevention of burn injuries by teaching ▪ Third-degree burn of burn <10% TBSA not involving special care areas
prevention concepts and promoting safety legislation. ▪ Excludes electrical injury, inhalation injury, or concurrent trauma and all
NATURE: poor-risk patients (eg, extremes of age, intercurrent disease)
3. MAJOR BURN INJURY
• 40%: flame related ▪ Second-degree burns >25% TBSA in adults or >20% in children
• 30%: scald injuries: occurs more often in children particularly the toddlers ▪ All third-degree burns >10% TBSA
• 4%: electrical ▪ All burns involving eyes, ears, face, hands, feet. Perineum, joints
• 3%: chemical ▪ All inhalation injury, electrical injury, or concurrent trauma, and all poor-risk
patients
GOALS RELATED TO BURNS:
METHODS TO ESTIMATE TOTAL BODY SURFACE AREA (TBSA) BURNED:
• Prevention
▪ Institution of life-saving measures for the severely burned person • Rule of nines – quick way; the system assigns percentages in multiples of
▪ Prevention of disability and disfigurement through early specialized and nine to a major body surface
individualized car
▪ Rehabilitation through reconstructive surgery and rehabilitation programs

CLASSIFICATION OF BURNS:

• Superficial Partial Thickness

1st degree – involves epidermis,
reddish, painful

ZONES OF BURN INJURY:

• Deep Partial Thickness
2nd degree – involves dermis.
Moist surface, with vesicles,
painful
• Lund and Browder method – more precise method; recognizes that the
percentage of surface area of various anatomic parts, esp. the head & legs,
changes with growth

• Full Thickness
▪ 3rd degree – involves
subcutaneous layer, pearly
white, no pain
▪ 4th degree – involves the
muscles and bones, blackish or
charred, no pain
FACTORS TO CONSIDER IN DETERMINING BURN DEPTH:

• How the injury occurred

• Causative agent
• Temperature of agent
• Duration of contact with the agent
• Thickness of the skin
 - More precise: recognizes that the percentage of TBSA of various anatomic B. Acute Phase
parts, especially the head and legs, and changes with growth ▪ Fluid re-enters the vascular space from the interstitial space.
- initial evaluation is made on the patient’s arrival at the hospital and is ▪ Hemodilution (↓HCT)- results as fluid enters the IVC; loss of RBCs dt lysis
revised within the 1st 72 hours at burn site
• Palm method – scattered burns; 1 size of palm is approximately 1% of the ▪ Increased urinary output-Fluid shift into IVC increases renal blood flow and
TBSA causes increased urine formation
▪ Hyponatremia: Sodium is lost with diuresis and due to dilution as fluid
PATHOPHYSIOLOGY OF BURNS: enters vascular space
• Burns are caused by a transfer of energy from a heat source to the body. ▪ Potential Hypokalemia: Potassium shifts from extracellular fluid into cells
• Thermal – hot objects or substances; due to fires in the home, auto accidents, ▪ Metabolic acidosis
playing with matches, poorly stored gas, faulty electrical systems, space CARDIOVASCULAR ALTERATIONS:
heaters, fire crackers, kitchen accidents, scalding
• Chemical – caused by contact, ingestion, inhalation, injection of strong acids • ↓ Cardiac Output even without significant changes in blood volume
or alkali • SNS stimulation dt Burn Shock releases Adrenal corticoid hormones and
• Electrical – from contact with malfunctioning electrical appliances, wires, flash Catecholamines leading to vasoconstriction→ further ↓ in CO
electrical arcs from any high voltage power lines, machine and lightning • 24-36 Hrs (peak at 6-8H) = Fluid Leak
• Radiation – excessive exposure to sunlight ▪ ↓ Increases Blood volume
▪ ↓ Increased renal perfusion
BURN RELATED RESPIRATORY INJURIES: ▪ ↓ DIURESIS (up to 2 weeks)
• Smoke Inhalation – carbon monoxide CO (most common), released when • Anemia due to destruction of RBC (but HCT level is increased)
organic substances are burned; Colorless, odorless gas that combines with PULMONARY ALTERATIONS:
Hgb 200x more than O2 causing Tissue Hypoxia; Causes headache, EMERGENT OR RESUSCITATIVE PHASE: ON-THE-SCENE CARE
dizziness, confusion, syncope, coma, respiratory failure • Bronchoconstriction – Histamine, serotonin, thromoxane;
- Treatment: 100% O2 administration; Hyperbaric O2 chamber to reduce • Upper airway – above glottis; Edema • Prevent: Prevent injury to rescuer.
CO level • Inhalation below the glottis-decrease ciliary function, Hypersecretion, Severe • Stop: Stop injury, extinguish flames, cool the burn, irrigate chemical burns
• Smoke Poisoning – results from noxious chemicals formed in the burning mucosal edema, Bronchospasm, decrease surfactant leading to Atelectasis • Establish: ABCs, Establish airway, breathing, and circulation.
process and is prevalent with nonorganic subst. (plastic); decreases ciliary and Expectoration of CO → Acute Respiratory Failure • Start: Start oxygen and large-bore IVs
action in respiratory tract and mucosal edema, bronchospasm, carbon-flecked - Treatment: Intubation, Mechanical ventilation, • Remove: Remove restrictive objects and cover the wound.
sputum and then sloughing of the tracheobronchial mucosa with cough up of • Carbon monoxide poisoning • Do: Do assessment, surveying all body systems, and obtain a history of the
purulent mucus • Restrictive defects – Escharotomy incident and pertinent patient history.
• Heat Injury – affects the upper airway with edema causing obstruction in the • Note: Note, Treat patients with falls and electrical injuries as for potential
RENAL ALTERATIONS: cervical spine injury.
first 24 to 48 hours after burn
• Due to dec Blood Volume, Hemolysis (Hgb in the urine), and Muscle Damage ✓ Patient is transported to emergency department.
PHYSIOLOGIC CHANGES: ✓ Rapid assessment; v/s q 15mins
(Myoglobin)
• Burns less than 20% TBSA produce a primarily local response. ▪ ↓ Occlusion of the renal tubules ✓ Maintain ABC; look for signs of inhalation injury
• Burns more than 20% may produce a local and systemic response and are ▪ ↓ Acute Tubular Necrosis ✓ Fluid resuscitation is begun
considered major burns. ▪ ↓ RENAL Failure ✓ Foley catheter is inserted
• Systemic response includes release of cytokines and other mediators into the ✓ Patients with burns exceeding 20-25% should have an NG tube inserted and
IMMUNOLOGIC ALTERATIONS: placed to suction.
systemic circulation.
• ✓ Patient is stabilized and condition is continually monitored
• Fluid shifts and shock result in tissue hypoperfusion and organ hypofunction. Diminished resistance to infection
▪ ↓ SEPSIS ✓ Address pain; only IV medication should be administered.
EFFECTS OF MAJOR BURN INJURY: ✓ Psychosocial consideration and emotional support should be given to patient
• Abnormal inflammatory factors, altered level of IgA, impaired neutrophil
and family
• Fluid and electrolyte shifts functions, decrease Lymphocytes
• Cardiovascular effects ▪ ↓ Immunosuppression MANAGEMENT OF SHOCK: FLUID RESUSCITATION:
• Pulmonary injury • Loss of skin integrity
• Release of abnormal inflammatory factors, altered levels of immunoglobulin • Maintain BP above 100 mm Hg systolic and urine output of 0.5- 1.0mL/kg/hr.
▪ Upper airway
Maintain serum sodium at near-normal levels.
▪ Inhalation below the glottis and serum complement, impaired neutrophil function, lymphocytopenia
• Consensus formula
▪ Carbon monoxide poisoning
GI ALTERATIONS: ▪ Lactated Ringer’s Solution (or other balanced saline solution)
▪ Restrictive defects
• Renal and GI alterations • ↓peristalsis and Bowel sounds 2-4 mL x kg body weight x % TBSA burned
• Immunologic alterations • Gastric distention and Nausea = vomiting Half to be given in 1st 8 hours Remaining half to be given over next
• Effect upon thermoregulation • Gastric bleeding due to massive physiologic stress= CURLING’s ulcer (acute 16 hours
ulcerative duodenal dse. 24 H post burn)
FLUID AND ELECTROLYTE SHIFTS:
PHASES OF BURN INJURY: • Evans formula
A. Emergent Phase
▪ Colloids: 1mL x kg body weight x %TBSA
▪ Generalized DHN-evaporative loss, fluid shift A. Emergent or resuscitative phase
▪ Electrolytes (Saline): 1mL x kg body weight x %TBSA
▪ Extensive local edema-maximal 24H, begins to resolve 1- 2days; - Onset of injury to completion of fluid resuscitation
▪ Glucose (5% in water): 2000 mL for insensible loss
completely resolved 7-10days B. Acute or intermediate phase
Day 1: Half to be given in the first 8 hours and the remaining half over
▪ Reduced blood volume and hemoconcentration - From beginning of diuresis to wound closure
next 16 hours
▪ Decreased urine output C. Rehabilitation phase
Day 2: Half of previous day’s colloids and electrolytes
▪ Trauma causes release of potassium into extracellular fluid: hyperkalemia - From wound closure to return to optimal physical and psychosocial
• Brooke Army formula
▪ Sodium traps in edema fluid and shifts into cells as potassium is released: adjustment
▪ Colloids: 0.5 mL x kg body weight x % TBSA burned
hyponatremia
▪ Electrolytes (lactated Ringer’s solution): 1.5 mL x body weight x %
▪ Metabolic acidosis
TBSA burned
 ▪ Glucose (5% in water): 2000 mL for insensible loss ▪ To remove tissue contaminated by bacteria and foreign bodies, thereby WOUND GRAFTING:
Day 1: Half to be given in first 8 h; remaining half over next 16 h. protecting the patient from invasion of bacteria.
• Purposes: to decrease risk of infection
Day 2: Half of colloids; half of electrolytes; all of insensible fluid ▪ To remove devitalized tissue or burn eschar in preparation for grafting and
replacement. wound healing. • to prevent further loss of protein, fluids &electrolytes
▪ Second and third-degree (partial- and full-thickness) burns exceeding 50% • to minimize heat loss through evaporation
ESCHAROTOMY: • permits earlier functional ability
TBSA are calculated on the basis of 50% TBSA
• Parkland Baxter formula • treat full thickness (third-degree) circumferential burns • reduces wound contractures
▪ Lactated Ringer’s solution: 4 mL x kg body weight x % TBSA burned • used primarily to combat compartment syndrome • temporary grafting is done before patient’s own skin is possible
Day 1: Half to be given in first 8 h; half to be given over next 16 h • performed by making an incision through the eschar (dead tissues) to expose • main areas for grafting are the face, hands and feet, and areas that involve
Day 2: Varies. Colloid is added. the fatty tissue in order to lessen its pull on the surrounding tissue. joint
• Hypertonic saline formula • granulation process to take place first before grafting
▪ Concentrated solutions of sodium chloride (NaCl) and lactate with TOPICAL ANTIBACTERIAL AGENTS FOR BURNS:
concentration of 250 -300 mEq of sodium per liter, administered at a rate • Silver Sulfadiazine 1%(Silvadene)- bactericidal agent
sufficient to maintain a desired volume of urinary output. Do not increase ▪ Minimal penetration of the eschar
the infusion rate during the first 8 postburn hours. Serum sodium levels ▪ Apply 1/16-inch layer of cream with sterile glove 1-3x/day
must be monitored closely. Goal: increase serum sodium level and - Nursing Implications:
osmolality to reduce edema and prevent pulmonary complications. ▪ Leucopenia 2-3days
• Note: Adjust formulas to reflect initiation of fluids at the time of injury. ▪ Pseudoeschar formation
NURSING MANAGEMENT: • Mafenide Acetate 5%-10% (Sulfamylon)
✓ Effective against gram – or + microorganism Diffuses rapidly through the
✓ Monitor v/s closely, (RR, PR, BP) eschar
✓ Monitor I&O ✓ In 10% strength, it is the agent of choice for electrical burns because of its
✓ Asses frequently urine specific gravity, glucose, protein, hgb; Burgundy colored ability to penetrate the eschar
urine suggests presence of hemochromogen & myoglobin due to muscle ✓ Apply thin layer with sterile glove 2x daily and leave open as prescribed; if
damage the wound is dressed, change q6h as prescribed
✓ Elevate burned extremity - Nursing Implications:
✓ Monitor IV therapy, obtain infusion pump ▪ Monitor ABG levels because it causes metabolic acidosis with its effect
NURSING PROCESS: CARE OF THE PATIENT IN THE EMERGENT PHASE OF on renal buffering
BURN CARE: DIAGNOSIS ▪ Analgesic for pain mgt- may cause pain
• Silver Nitrate- Bacteriostatic and fungicidal
• Impaired gas exchange ✓ Does not penetrate the eschar
• Ineffective airway clearance ✓ Apply to gauze dressing, place over wound. Keep dressing wet but
• Fluid volume deficit covered w/ dry gauze & blankets to prevent vaporization. Re-moisten q2h;
• Hypothermia redress wound 2x daily
• Acute pain - Nursing Implications:
• Anxiety ▪ Monitor Na & K serum levels because of its hypotonicity
▪ Protect bed linen/clothing in contact as it causes black staining
ACUTE OR INTERMEDIATE PHASE: • Acticoat- Effective against gram – or + microorganism and some yeasts and
• Begins 48-72 hrs. after the burn injury molds
• Priorities of care: Continued assessment and maintain respiratory and ✓ Delivers a uniform, antimicrobial concentration of silver to the burn wound
circulatory support; F&E balance, prevention of infection, wound care, pain ✓ Moisten w/sterile water only; Apply directly to wound.
management, and nutritional support ✓ Cover with absorbent secondary dressing. Remoisten w/ sterile water q3-
• Cautious administration of fluid because of fluid shifts from the interstitial to the 4h.
intravascular compartment, losses of fluid from large burn wounds - Nursing Implications:
• Fever: caused by bacteremia and septicemia; treated with acetaminophen and ▪ No oil-based products or topical antimicrobials
hypothermia blanket ▪ Keep moist
▪ Left in place 3-5 days
• Continued Assessment of Circulatory Status, F&E:
▪ Hemodilution • Other agents:
▪ Increased UO ▪ Aquacel, Siversorb, Silverlon, Povidone-iodine ointment 10%; gentamicin
▪ Hyponatremia sulfate; nitofurazone; Dakin’s solution; acetic acid; miconazole;
▪ Hypokalemia clotrimazole Bacitracin is used for facial burns
▪ Acidosis ✓ Wound dressing, dressing changes
▪ Continuous and monitored fluid resuscitation ✓ light dressing for joints areas (allow motion); areas with splint (maintain body
contour); on face (absorb exudates going into the eyes)
BURN WOUND CARE: ✓ circumferential dressings applied from distal to proximal; fingers and toes
wrapped individually
A. Wound cleaning – Hydrotherapy-cleaning of wounds & exercising the
✓ burns on face left open to air
extremities.
✓ occlusive dressings are used over areas with new skin, graft; this thin gauze
✓ The temperature of the water is maintained at 37.8 C (100 F)
with antimicrobial agent remains in place for 3-5 days
✓ The temperature of the room should be maintained between 26.6 C and
✓ changing of dressings is done 20 minutes after analgesic agent is prescribed
29.4 C (80 oF to 85 oF)
✓ note for color, odor, size, exudates, signs of re-epithelialization, eschar and
✓ Limited to a 20–30-minute period to prevent chilling and additional
other changes
metabolic stress.
✓ peripheral extremities must be checked frequently and burned areas elevated
B. Wound debridement – the removal of foreign material and devitalized tissue
on 2 pillows
until surrounding healthy tissue is exposed; two goals:
COMPARISON OF INTEGRA TEMPLATE AND SPLIT-THICKNESS AUTOGRAFT: ▪ High Carbohydrates (55%-85%) NURSING DIAGNOSIS:
▪ Low fat (3%-20%)
A. Activity intolerance r/t pain on exercise, limited joint mobility, muscle wasting,
• Vitamin supplementation:
and limited endurance
▪ A: skin & mucous membrane integrity
NI: Promoting Activity Tolerance
▪ B: enhances metabolism
• Insomnia due to frequent nightmares (listening; prescribed hypnotic
▪ C: ↑ resistance to stress & infection
agents)
• Oral fluids must be initiated slowly
• Metabolic stress (relieve pain; preventing chilling or fever)
• High protein and high vitamin food
• Muscle atrophy (therapy exercises)
• High calorie nutritional supplements
• Low endurance (play therapy)
• Vitamins and Mineral supplements
• Enteral feeding of bolus formula if not possible by mouth EO: Obtains adequate sleep daily
• Parenteral nutrition if GI function is compromised
• Reports absence of nightmares or sleep disturbance
• Weigh patient daily and record
• Shows gradually increasing tolerance and endurance in physical activities
CARE OF THE GRAFT SITE: DISORDERS OF WOUND HEALING: • Can concentrate during conversations
• Has energy available to sustain desired daily activities
• Use of occlusive dressings to immobilize the graft. A. Hypertrophic scars: form within the boundaries of the initial wound and push
B. Disturbed body image r/t altered physical appearance and self-concept or
• First dressing change is performed 2-5 days after surgery. outward on the perimeter of the wound.
Impaired coping
• Sterile saline to prevent drying of the graft. - Areas over joints
NI: Improving Body Image and Self-concept
• Patient positioned and tuned carefully to avoid disturbing the graft - Hypopigmented/hyperpigmented
• Refer patient to support group
• Elevate grafted extremity to minimize edema. B. Scars: red, raised and hard
• Meet others with same experience and learn coping strategies
• Patient to exercise the grafted area 5-7 days after grafting. - Prevention and Treatment of Scars:
▪ Compression: early in burn wound treatment • Constantly assess the patient’s psychological reactions
CARE OF THE DONOR SITE (AREA FROM WHICH SKIN IS TAKEN): → Elastic Bandage wraps: desensitize the patient’s skin, protect healing ▪ EO: Verbalizes alterations in body image and accepts physical
appearance
• Moist gauze dressing applied after surgery to maintain pressure and stop areas, apply pressure, and promote venous return
• Demonstrates interest in resources
bleeding. → Elastic pressure garments: loosens collagen bundles and
encourages parallel orientation of the collagen to the skin surface • Use cosmetic; wigs; and prostheses;
• Thrombostatic agents applied to the site. • Socialize with others
• Covering of donor sites with biosynthetic dressings. → Worn 23 hrs a day
▪ Silicone Sheets: for small troublesome areas • Seeks and achieve family and societal roles
• Pain relievers. C. Deficient knowledge about post-discharge home care and follow-up needs
▪ Gentle superficial scar massage w/ moisturizer: smaller areas
*A donor site heals within 7-14 days with proper care NI: Demonstrate knowledge of required self-care and follow-up care
▪ Steroid injections
PAIN MANAGEMENT: C. Keloid: irregularly formed scar, extends beyond the margins of the original EO: Describes surgical procedures and Tx accurately
wound • Verbalizes detailed plan for follow-up care
• Burn pain has been described as one of the most severe forms of acute pain. • Demonstrate ability to perform wound care and prescribed exercises
- Large, nodular, ropelike
• Pain accompanies care and treatments such as wound cleaning and dressing • Returns for follow up appointments
- Itchy, tenderness
changes. • Identifies resource people and agencies to contact for specific problems
D. Contractures: burn wound tissue shortens because of the force exerted by
• Types of burn pain
the fibroblasts
▪ Background or resting: exists on 24-hour basis OTHER MAJOR CARE ISSUES:
- and the flexion of muscles in natural wound healing
▪ Procedural: caused by manipulation of wound bed during dressing
- Tx: splints, traction, and purposeful movement and positioning: counteract • Pulmonary care
changes or ROM exercises
deformity in burns affecting joint • Psychological support of patient and family
▪ Breakthrough: occurs when blood levels of analgesic agents decreased
• Patient and family education
below the level required CARE OF THE PATIENT DURING ACUTE PHASE:
• Restoration of function
• Analgesics
A. Assessment:
▪ IV use during emergent and acute phases POTENTIAL COMPLICATIONS/COLLABORATIVE PROBLEMS:
• Focuses on hemodynamic alterations, wound healing, pain and
▪ Morphine
psychosocial responses, early detection of complications. • Acute respiratory failure
▪ Fentanyl
• Frequent assessment on vital signs, peripheral pulses, edema, • Distributive shock
▪ Other
dysrhythmias, electrolyte imbalance, residual gastric volumes, and pH. • Distributive shock
• Role of anxiety in pain
• Assess burn wounds as to size, color, odor, eschar, exudates, abscess • Compartment syndrome
• Effect of sleep deprivation on pain
formation, epithelial buds bleeding, granulation, status of grafts and donor • Paralytic ileus
• Nonpharmacologic measures Relaxation techniques; deep breathing
sites, and quality of surrounding skin. • Curling’s ulcer
exercises, distraction, guided imagery, hypnosis, therapeutic touch, humor, and
• Focus on pan and psychosocial responses, daily weights, caloric intake,
information giving, music therapy REHABILITATION PHASE:
general hydration, serum electrolytes, Hgb and Hct levels.
NUTRITIONAL SUPPORT: • Rehabilitation is begun as early as possible in the emergent phase and
NURSING PROCESS: CARE OF THE PATIENT IN THE ACUTE PHASE OF BURN
• Burn injuries produce profound metabolic abnormalities. Patients with burns CARE: DIAGNOSIS extends for a long period after the injury.
have great nutritional needs related to stress response, Increased catabolic • Focus is upon wound healing, psychosocial support, self-image, lifestyle, and
• Excessive fluid volume restoring maximal functional abilities so the patient can have the best-quality
hormones (cortisol and catechols), hypermetabolism, and wound healing.
• Risk for infection life, both personally and socially.
• Goal of nutritional support is to promote a state of nitrogen balance and match
• Imbalanced nutrition • The patient may need reconstructive surgery to improve function and
nutrient utilization.
• Acute pain appearance.
• Nutritional support is based on patient’s pre-burn status and % of TBSA
• Impaired physical mobility • Vocational counseling and support groups may assist the patient
burned.
• Ineffective coping
• Enteral route is preferred. Jejunal feedings are frequently used to maintain
nutritional status with lower risk of aspiration in a patient with poor appetite, • Interrupted family processes
weakness, or other problems. • Deficient knowledge
• Calories:
▪ High Protein (15%-25%): 2-3g/kg BW/every 24 hours
COMPLICATIONS IN REHABILITATION PHASE OF BURN CARE: • Constantly assess the patient’s psychological reactions
A. Neuropathies, nerve entrapment: Electrical injury, large deep burns, EO: Verbalizes alterations in body image and accepts physical
improper positioning, edema, scar tissue appearance
Nursing Interventions:
• Demonstrates interest in resources
• Assess peripheral pulses and sensation.
• Use cosmetic; wigs; and prostheses
• Prevent edema and pressure by elevation, positioning, prevention of
constricting dressings. • Socialize with others
• Assess splints for proper fit and application. • Seeks and achieve family and societal roles
C. Deficient knowledge about post-discharge home care and follow-up needs
• Consult OT and PT for positioning.
NI: Demonstrate knowledge of required self-care and follow-up care
B. Heterotopic ossification: Prolonged immobility – abnormal formation of true
EO: Describes surgical procedures and treatment accurately
bone within extraskeletal soft tissues
Nursing Interventions: • Verbalizes detailed plan for follow-up care
• Perform gentle range-of-motion exercises • Demonstrate ability to perform wound care and prescribed exercises
C. Hypertrophic scarring: Partial and full-thickness burns • Returns for follow up appointments
Nursing Interventions: • Identifies resource people & agencies to contact for any problem
• Keep skin pliable and soft. HOME CARE INSTRUCTIONS:
• Apply pressure garments as prescribed.
• Massage. • Mental health
D. Contractures: Partial and full-thickness burns • Skin and wound care
Nursing Interventions: • Exercise and activity
• Maintain position of joints in alignment. • Nutrition
• Perform gentle range-of-motion exercises. • Pain management
• Consult OT and PT for exercises and positioning recommendations. • Thermoregulation and clothing
E. Wound breakdown – sheer, pressure, inadequate nutrition • Sexual issues
Nursing Interventions:
COLLABORATIVE PROBLEMS/POTENTIAL COMPLICATIONS:
• Teach patient about importance of good nutrition.
• Protect wound from pressure and shearing forces. • Heart failure and pulmonary edema
F. Gait deviations: Pain; burn wound; donor site, scarring of joints, electrical • Sepsis
injury of the brain • Acute respiratory failure
Nursing Interventions: • Visceral damage (electrical burns)
• Provide adequate pain management.
• Consult OT and PT.
• Promote ambulation and mobility training.
G. Complex regional pain syndrome: Trauma and burns
Nursing Interventions:
• Provide adequate pain management.
• Consult OT and PT for exercises.
• Promote gentle motion of affected extremities.
H. Joint instability: Burn wound, burn scar, and contractures
Nursing Interventions:
• Maintain joint through appropriate application of splints.
• Monitor joint pinning if indicated.
• Consult OT and PT

NURSING DIAGNOSES:

A. Activity intolerance r/t pain on exercise, limited joint mobility, muscle wasting,
and limited endurance
NI: Promoting Activity Tolerance
• Insomnia due to frequent nightmares (listening to patients; administer
prescribed hypnotic agents)
• Metabolic stress (relieve pain; preventing chilling or fever)
• Muscle atrophy (therapy exercises)
• Low endurance (play therapy)

EO: Obtains adequate sleep daily

• Reports absence of nightmares or sleep disturbance

• Shows gradually increasing tolerance and endurance in physical activities
• Can concentrate during conversations
• Has energy available to sustain desired daily activities
B. Disturbed body image r/t altered physical appearance and self-concept
NI: Improving Body Image and Self-concept
• Refer patient to support group
• Meet others with same experience and learn coping strategies
 #9 FLUIDS & ELECTROLYTES: BALANCE AND DISTURBANCES
FLUID:
- “Third spacing”: loss of ECF into a space that does not contribute to
equilibrium
→ Early evidence: decreased UO despite adequate fluid intake
→ E.g. ascites, burns, peritonitis, bowel obstruction, massive bleeding into
a joint or body cavity
BLOOD VESSEL W/ SURROUNDING TISSUE: ▪ Osmotic pressure – exerted by the protein in the plasma (oncotic
pressure); the amount of hydrostatic pressure needed to stop the flow of
water by osmosis
NOTE: THE DIRECTION OF FLUID MOVEMENT DEPENDS ON THE
DIFFERENCES OF HYDROSTATIC PRESSURE AND OSMOTIC PRESSURE.
• Osmosis
- Movement of fluid from a region of low solute concentration to the region of
high solute concentration until the solutions are of equal concentration
- The magnitude of osmosis depends on the number of particles dissolved in
the solution, which influences the movement of fluid between
compartments.
- Tonicity: ability of solutes to cause an osmotic driving force promoting
water movement from one compartment to another
- Oncotic pressure: the osmotic pressure exerted by proteins
- Osmotic diuresis: increase in UO caused by the excretion of substances
such as glucose, mannitol, or contrast agents in the urine
REGULATION OF FLUID:
• Normal movement of fluids through capillary walls into tissues depends on:
▪ Hydrostatic pressure – pressure exerted by the fluid on the walls of blood
vessel at the arterial & venous ends when it is at rest
• Diffusion
- Natural tendency of molecules and ions to move from an area of higher
concentration to an area of lower concentration
- Ex: O2 & CO2 exchange, tendency of sodium movement from ECF to ICF
 • Filtration - Cortisol: produce sodium & fluid retention & potassium deficit (less
- Movement of water and solutes from an area of higher hydrostatic pressure mineralocorticoid activity)
to an area of lower hydrostatic pressure • Parathyroid glands Functions – regulate calcium & phosphate balance
- Ex.: Fluid from intravascular to interstitial space from the pumping action of • Pituitary gland Functions – Storage of ADH
the heart

LAB TESTS FOR EVALUATING FLUID STATUS:

• Active Transport
• Osmolality- the total number of dissolved particles per kg; controls water OTHER MECHANISMS:
- Physiologic pump that moves fluid from an area of lower concentration to
movement between & within body fluid compartments
one of higher concentration • BARORECEPTORS
▪ Serum osmolality – 280 – 300 mOsm/kg
- Movement is against a concentration gradient - Detect changes in pressure within blood vessels
▪ Urine osmolality – 200 – 800 mOsm/kg; determined by urea, creatinine,
- Sodium-potassium pump maintains the higher concentration of - Regulate sympathetic & parasympathetic neural activity as well as
and uric acid
extracellular sodium and intracellular potassium endocrine activities
• Osmolarity – the total number of dissolved particles per liter of solution
- Requires adenosine (ATP) for energy
• Urine specific gravity – 1.010 to 1.025
- Less reliable indicator of concentration than urine osmolality because
increased glucose or protein can falsely elevate values
• BUN – end product of protein metabolism (from both muscle & dietary intake)
by the liver
- N = 10 – 20 mg/dL increase
- BUN: decreased renal function, GI bleeding, DHN, increased protein
intake, fever, and sepsis
- Decrease BUN: end-stage liver disease, low protein diet, starvation
• Creatinine – end product of muscle metabolism
- N = 0.7 – 1.4 mg/dL
• Hematocrit – measures the volume percentage of RBC in whole blood
- N= males 42% - 52%; females 35% - 47%
• Urine Sodium – assess volume status, sodium imbalances and acute renal
failure
- N= 50-220 mEq/24h

HOMEOSTATIC MECHANISMS: ORGANS INVOLVED

• Kidney Functions
- Regulation of ECF volume & osmolality by selective retention & excretion
of body fluids
- Regulation of electrolyte levels in the ECF • OSMORECEPTORS – sense changes in sodium concentration then causes
- Regulation of pH of the ECF release of ADH
- Excretion of metabolic wastes & toxic substances • RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM – aldosterone released
ROUTES OF GAINS AND LOSSES:
• Lung Functions with: decreased Na, increased K, and increased ACTH
• Gains - Sensible loss through exhalation
- Dietary intake of fluid and food or enteral feeding - Maintain acid-base balance
- Parenteral fluids • Heart & Blood Vessel Functions
- Pumping action of heart allows urine formation
- Failure of the pumping action interferes with renal perfusion and water &
electrolyte regulation
• Adrenal glands Functions
- Aldosterone: Na and water retention, K loss
 ▪ Dehydration – loss of water alone with increased serum sodium level ▪ Fluid challenge Test: if oliguric
- CAUSES: → Volumes of fluid administered at specific rates & intervals while the
→ Loss of body fluids - vomiting, diarrhea, GI suctioning, sweating patient’s hemodynamic response is monitored
→ decreased intake, - nausea, lack of access to fluids → 100 to 200 mL of NSS over 15 mins ⇢ ⇧ UO, ⇧ BP and CVP
→ Third-space fluid shifts ˗ NURSING MANAGEMENT ASSESSMENT:
- RISK FACTORS: diabetes insipidus, adrenal insufficiency, osmotic ▪ I&O
diuresis, hemorrhage, coma ▪ weight
- CLINICAL MANIFESTATIONS: ▪ VS
▪ Acute weight loss ▪ skin and tongue turgor, mucous membranes
▪ decreased skin turgor ▪ Urine concentration
▪ oliguria ▪ Mental status
▪ concentrated urine ▪ s/s of decreased peripheral tissue perfusion
▪ postural hypotension ▪ PREVENT HYPOVOLEMIA
▪ rapid and weak pulse → Identify patients at risk
▪ Flat neck veins → Minimize fluid loss
▪ increased temperature → Diarrhea – antidiarrheal agents, fluids at frequent intervals
▪ Delayed CRT ▪ CORRECT HYPOVOLEMIA
▪ Decreased CVP → Oral fluids
▪ cool and clammy skin → Frequent mouth care
▪ lassitude, anorexia nausea, muscle weakness, and cramps → Provide nonirritating fluids
▪ Shock (>25%lost/rapid) → Oral rehydration solutions
→ Nausea - antiemetics
• FLUID VOLUME EXCESS (FVE): HYPERVOLEMIA
• RELEASE OF ATRIAL NATRIURETIC PEPTIDE - Isotonic expansion of the ECF caused by the abnormal retention of water
- Released by the atrial cells in response to increase atrial pressure, angio II, and sodium
endothelin, & sympa stimulation - CAUSES: fluid overload or diminished function of homeostatic mechanisms
- Action is the direct opposite of Renin-angiotensin-Aldosterone system & - RISK FACTORS: heart failure, renal failure, and cirrhosis of the liver
decreases blood pressure & volume - CONTRIBUTING FACTORS: excessive dietary sodium or sodium-
containing IV solutions
- CLINICAL MANIFESTATIONS:
▪ edema
▪ distended neck veins
▪ abnormal lung sounds
▪ tachycardia, increased BP, pulse pressure, and CVP
▪ increased weight
▪ increased UO
▪ shortness of breath and wheezing
- ASSESSMENT & DIAGNOSTIC FINDINGS:
▪ BUN & HCT are decreased
▪ Serum osmolality and sodium levels decreased
▪ Chest X-Ray - pulmonary congestion
- MEDICAL MANAGEMENT:
▪ Directed at the cause restriction of fluids and sodium, and the
- ASSESSMENT & DIAGNOSTIC FINDINGS: administration of diuretics
▪ elevated BUN to creatinine ratio a. Restriction of fluids & sodium
▪ increased hematocrit, b. Diuretics
▪ possible serum electrolyte changes Thiazide for mild to moderate hypervolemia
→ Hypokalemia – GI & renal losses Loop diuretics for severe hypervolemia S/E: Hypokalemia,
→ Hyperkalemia: - adrenal insufficiency Hyperkalemia, Hyponatremia, Hypomagnesemia
→ Hyponatremia - increased thirst & ADH release c. Hemodialysis, PD
• ADH & THIRST → Hypernatremia - increased insensible losses & diabetes insipidus d. Nutritional Therapy
- Maintain sodium concentration & oral intake of fluids ▪ Increased urine specific gravity and urine osmolality
- Released with: increased serum osmolality or decrease in blood volume - GERONTOLOGIC CONSIDERATIONS:
▪ ⇧ sensitivity to F&E changes
GERONTOLOGIC CONSIDERATIONS:
▪ Alterations in skin elasticity
• Reduced homeostatic mechanisms: cardiac, renal, and respiratory function ▪ Changes in ability to determine/meet food & fluid needs
• Decreased body fluid percentage - MEDICAL MANAGEMENT:
• Medication use ▪ provide fluids to meet body needs
• Presence of concomitant conditions ▪ Oral fluids
▪ IV fluids
FLUID VOLUME IMBALANCES: → Isotonic solution: e.g., Lactated Ringer’s or 0.9% NaCl
• FLUID VOLUME DEFICIT (FVD): HYPOVOLEMIA → Hypotonic solution: e.g., 0.45% NaCl
- Loss of ECF volume exceeds intake of fluid; Water and electrolytes are lost once patient is normotensive
in the same proportion – ratio of serum electrolytes to water remains the Provide water & electrolytes for renal excretion of metabolic
same wastes
 - NURSING MANAGEMENT: Diuretics → MANIFESTATIONS:
▪ I&O and daily weights; assess for lung sounds non-renal: vomiting, diarrhea, sweating primarily neurologic and ↑plasma osmolality
▪ Edema – check for indentation; measure circumference dilutional hyponatremia: ECF volume increased without any leads to a concentrated ECF
▪ monitor responses to medications such as diuretics edema a. Primary characteristic: Thirst (may be impaired in elderly &
▪ sodium and fluid restrictions adrenal insufficiency ill)
✓ Avoid foods high in Na SIADH b. Moderate hypernatremia – restlessness and weakness
✓ Avoid OTC meds Hyperglycemia increase H2O intake c. Severe hypernatremia – disorientation, delusions, and
✓ Light salting of food use of tap-water enemas hallucinations; permanent neurologic damage can occur
✓ Read food labels irrigation of NGT with water slightly elevated temperature; dry, swollen tongue; sticky
✓ Use Seasoning substitutes: lemon juice, onions, garlic Compulsive H2O drinking mucosa; neurologic symptoms; restlessness; weakness;
✓ Use salt substitutes with caution: contain K! ammonium chloride! → CLINICAL MANIFESTATIONS: postural hypotension, oliguria; flushed skin, peripheral &
✓ Use distilled water Poor skin turgor, dry mucosa, headache, decreased salivation, pulmonary edema
✓ Avoid water softeners decreased BP, nausea, abdominal cramping → LABORATORY FINDINGS:
- NURSING INTERVENTIONS: Neurologic changes: altered mental status, status epilepticus & Serum sodium level > 145 mEq/L
▪ Teach about edema: coma; obtundation Serum osmolality >300 mOsm/Kg
▪ Causes Anorexia, muscle cramps, feelings of exhaustion Increased urine specific gravity and urine osmolality
a. Increased capillary fluid pressure When serum Na level decreases to < 115 mEq/L – increased → MEDICAL MANAGEMENT:
b. Decreased capillary oncotic pressure – decreased albumin ICP; lethargy; confusion; muscle twitching; focal weakness; a. Hypotonic electrolyte solution (0.3% NaCl) or isotonic solution
c. Increased interstitial oncotic pressure- obstruction to lymphatic flow hemiparesis; pappiledema; seizures (D5W)
d. Meds: NSAIDS, corticosteroids, antihypertensives → LABORATORY FINDINGS: b. Diuretics
▪ Localized or generalized; ascites Serum sodium- 1.012 & urine Na >20mEq/L c. Desmopressin acetate (DDAVP) – a synthetic ADH for
▪ Elevate edematous extremities SIADH: ➔ Se Na as low as 100 mEq/L; ➔ ↑ specific gravity treatment of hypernatremia due to DI
▪ Use semi-Fowler’s position for orthopnea >1.012 & urine Na >20mEq/L → NURSING MANAGEMENT:
▪ skin care and positioning/turning Serum osmolality – 250 mOsm/kg (diluted) Assess use of OTC drugs (e.g. Alka-Seltzer)
Low Specific gravity 1.002-1.004 (overdehydrated) Adequate fluid intake and water with tube feedings
ELECTROLYTE BALANCE & IMBALANCE:
→ MEDICAL MANAGEMENT: Prevention: Offer fluids at regular intervals. Unconscious
ELECTROLYTES: a. Sodium replacement: patients by alternative routes
Na administration (oral, NGT, parenteral) - Should not For Diabetes insipidus- adequate water intake must be ensured
- Active chemicals that carry positive (cations) and negative (anions)
exceed 12 mEq/L/24hrs (neurologic damage due to osmotic To correct hypernatremia: Parenteral fluids, monitor on serum
electrical charges
demyelination) sodium levels and monitor neurologic changes
- Major cations:
Dietary intake of Na • POTASSIUM: hypokalemia and hyperkalemia
▪ Sodium
Infusion of Lactated Ringer’s solution or isotonic saline (0.9 ˗ Potassium (K+) 3.5-5.0 meq
▪ Potassium
% sodium chloride) ˗ Assist in regulation of intracellular osmolality
▪ Calcium
b. Water restriction ˗ Necessary for cellular growth and metabolism
▪ Magnesium
LOF: 800 mL/day ˗ Helps promote conduction of impulses
▪ Hydrogen ions
Administer small amount of a hypertonic sodium solution, 3 ˗ Helps promote proper function of skeletal & cardiac muscle activity
- Major anions:
% to 5 % NaCl if neurologic symptoms are present ˗ moves into cells when: glucose is metabolized; during beta adrenergic
▪ Chloride
= administered slowly and in small volumes stimulation; during alkalosis
▪ Bicarbonate
= monitored closely for fluid overload ˗ moves out of the cells during: strenuous exercise; cellular metabolism is
▪ Phosphate
= patient receives a loop diuretic to prevent ECF volume impaired; when cells die; during acidosis
▪ Sulfate
overload and to increase water excretion ˗ Regulation: Kidneys
▪ Proteinate ions
→ NURSING MANAGEMENT: ▪ HYPOKALEMIA:
- Electrolyte concentrations differ in the fluid compartments
Monitor I/O and daily weight. → ETIOLOGY:
- Expressed in milliequivalents (mEq)/L
Note abnormal losses of sodium or gains of water. a. Inadequate intake of K+ (dietary habits, nausea, anorexia;
- Electrolyte concentrations in the ICF differ from those in the ECF
Monitor GI manifestations acute alcoholism; extreme dieting; NPO orders; parenteral
- ICF:
Monitor neurological changes fluids are low in K+ and high in Na+)
▪ Cation: potassium
Encourage foods and fluids with a high sodium diet. b. Increased utilization of K+ during the healing phase of burns
▪ Anion: phosphates & sulfates
Observe lithium toxicity for patients taking lithium. c. Excessive loss of K+ (diuretics & antibiotics; adrenal steroid
- ECF:
Determine actual fluid needs – based on I&O, urine specific therapy; excessive infusions of saline solutions without K+
▪ Cation: Sodium
gravity, and serum sodium levels replacement; gastric & intestinal suction, operations involving
▪ Anion: Chloride
▪ HYPERNATEREMIA drainage from the surgical site like colostomies, ileostomies,
ELECTROLYTE IMBALANCES: → ETIOLOGY: large or small bowel resections)
Caused by a gain of sodium in excess of water or by a loss of d. Conditions of the GIT: vomiting & diarrhea
• SODIUM: hyponatremia and hypernatremia
water in excess of sodium (may occur with normovolemia, FVD e. Metabolic disorders like hyperaldosteronism; Cushing’s
- Sodium (Na) = 135 to 145 mEq/L syndrome; Insulin therapy
or FVE) – common: very old, very young & impaired patients
- Most abundant: ECF f. Alkalosis due to K shift into cell in exchange for hydrogen ion
Ingestion of more sodium than water
- Primary determinant of ECF volume and osmolality g. Renal disorders like nephropathies and diuretic phase of acute
Fluid deprivation (comatose)
- Control distribution of water throughout the body renal failure
Administration of hypertonic enteral feedings without adequate
- Regulated by: ADH, thirst, RAAS
water supplements → CLINICAL MANIFESTATIONS:
- Loss or gain is accompanied by a loss or gain of water a. Due to ↓ neuromuscular irritability- weakness; speech changes;
Watery diarrhea & ↑insensible water loss
- Establish the electromechanical state necessary for muscle contraction flaccid paralysis; shallow respirations; decreased intestinal
Diabetes insipidus or ADH deficiency
and transmission of nerve impulses motility; abdominal distention; anorexia; paralytic ileus
Heat stroke, near-drowning in sea water, malfunction of
▪ HYPONATREMIA b. Weakness of cardiovascular smooth muscle and prolongation
hemodialysis/peritoneal dialysis; IV administration of hypertonic
→ Serum sodium less than 135 mEq/L saline or excessive use of sodium bicarbonate of myocardial repolarization ◦ predisposes the patient to digitalis
→ CAUSES: toxicity
Imbalance of water rather than sodium
 c. Polyuria & nocturia- due to inability of kidneys to concentrate
urine
→ NURSING DIAGNOSES:
Alteration in urinary elimination patterns due to inability of
kidneys to concentrate urine
Anxiety and fear due to flaccid paralysis, shallow respirations,
and cardiac disturbances
Altered nutrition: less than body requirements due to anorexia
and paralytic ileus
Knowledge deficit involved in the administration of diuretics,
extreme dieting, & self-induced vomiting
→ MEDICAL MANAGEMENT:
Increase dietary potassium (50-100 meq/L)
Potassium replacement: Oral (Potassium Chloride, Potassium
Citrate, Potasssium Bicarbonate, Potassium Triplex) and IV for
severe deficit
➢ IV Potassium: administered only after adequate urine flow
has been established; stop infusion if urine volume is 20
ml/hr for 2 consecutive hours
❖ administered using an infusion pump and NEVER by IV
push or IM or IV drip
❖ Dilute well with PNSS
❖ the maximum concentration of potassium administered
is 20 mEq/100 ml and the rate no faster than 20
mEq/hour
→ PREVENTING HYPOKALEMIA:
Increase intake of K-rich foods  Educate: abuse of laxatives
and diuretics
Monitor I&O (40 mEq of potassium is lost every liter of urine
output)
Monitor ECG changes
→ NURSING MANAGEMENT:
Assess carefully (severe hypokalemia is life-threatening),
Monitor of electrocardiogram (ECG), arterial blood gases
(ABGs), and dietary potassium,
Provide nursing care related to IV potassium administration
▪ HYPERKALEMIA
→ (>5.0 meq/L)
→ Three major causes:
a. Retention of K+ in the body: renal failure, post-operative
individuals with poor urine output; with adrenocortical
insufficiency
b. Excessive release of potassium from cells: burns, traumatic
injuries, infection, or acidosis especially with reduced renal
function
c. Excessive intravenous infusions: rapid infusion of K+
also attributed by medications such as: KCl; heparin; ACE
inhibitors; captopril; NSAIDS and potassium sparing
diuretics
→ CLINICAL MANIFESTATIONS:
Cardiac effects: > 8 mEq/L = ECG changes ➔ dysrhythmias &
cardiac arrest
Skeletal muscle weakness & paralysis
Slowed ventricular conduction
Respiratory & speech muscle paralysis
GI manifestations: nausea, diarrhea
→ MEDICAL MANAGEMENT:
Decrease Potassium Intake- eliminate oral and parenteral
sources of K+
➢ Cation-exchange resins: sodium polysterene sulfonate
(Kayexalate)
➢ Severe: IV calcium gluconate (antagonizes the action of
hyperkalemia to the heart) – monitor BP
➢ IV administration of sodium bicarbonate (to alkalinize
plasma)
➢ IV insulin and a hypertonic dextrose solution (temporary
shift of K into cells)
→ NURSING MANAGEMENT:
Assess serum K Management + levels
Observe for signs of muscle weakness & dysrrhythmias,
paresthesias, GI symptoms
Mix well IVs containing K+
Monitor medication effects
Initiate dietary potassium restriction and dietary teaching for
patients at risk (food sources with minimal K+ content: butter,
margarine, cranberry juice, ginger ale, hard candy, rootbeer,
sugar, honey)
Use salt substitutes sparingly
Teach on K-sparing diuretics
• CALCIUM: hypocalcemia and hypercalcemia
- (8.6- 10.2 mg/dL)
- Distribution of Ca++: 99 % in bones; 1 % in plasma (ionized, bound,
complexed)
- Functions include:
a. Promotes normal neuromuscular irritability
b. Promotes normal muscular contractility
c. Promotes transmission of nerve impulses
d. Strengthens capillary membranes
e. Essential for blood clotting
f. Essential for building of bones and teeth
g. Essential for secretions of many hormones
- Calcium requirements:
✓ adult, at least 0.8 gm daily
✓ infants and children, 0.17 – 1.4 gm daily
✓ pregnant and lactating women, 1.3 – 1.5 gm daily
- Ca intake:
✓ ¾ supplied by milk and milk products
✓ ¼ supplied by vegetables and fruits
- Ca absorption:
✓ depends in part on presence of Vit. D
✓ controlled by parathyroid gland
- Ca excretion: in urine and feces
- Inverse relationship between Ca and Phosphorus
✓ when calcium is elevated, phosphorus is low
✓ when calcium is low, phosphorus is elevated
- Regulation of serum Ca
- controlled by PTH and calcitonin
▪ HYPOCALCEMIA
→ Serum level less than 8.5 mg/dL must be considered in conjunction
with serum albumin level
→ CAUSES: Excessive removal of Ca from the body due to acute
pancreatitis, diarrhea, hypoparathyroidism, and renal diseases;
Thyroidectomy with accidental removal of parathyroid glands;
Pregnancy and lactation (high demand of Calcium); Inadequate intake
of vitamin D; Following correction of acidosis and alkalosis
→ CLINICAL MANIFESTATIONS:
Increased neuromuscular irritability producing hyperaction of
motor and sensory nerves to stimuli:
Tetany - refers to the entire symptom complex induced by
increased neural excitability (same with hypomagnesemia)
tingling and numbness of fingers and circumoral regions; painful
tonic spasms; facial spasms/tetany facies; grimacing; fatigue;
laryngospasm; (+) Chvostek’s and Trosseau’s signs;
convulsions
mental changes (depression, impaired memory, confusion,
delirium, hallucinations)
hyperactive bowel sounds, dry and brittle hair and nails, abnormal
clotting for chronic hypocalcemia
Altered cardiac muscle function – definitive ECG tracing of
prolonged QT segment ; palpitations; arrythmias; torsades de
pointes (ventricular tachycardia)
→ LABORATORY TESTS:
Serum level below normal
Serum phosphorus elevated
Sulcowitch urine test(24 hr urine test) shows no precipitation
→ NURSING DIAGNOSES:
Acute pain due to tonic muscle spasms
Anxiety and fear r/t increased neuromuscular irritability, laryngospasm,
and impending tetany
Decreased cardiac outputr/t altered cardiac muscle function
Risk for injury r/t increased neuromuscular irritability
→ MEDICAL MANAGEMENT: corrected by oral, IM, IV CA salts:
Calcium lactate, Calcium gluceptate, Calcium chloride- do not
administer IM because it irritates tissues
Calcium gluconate
✓ administered slowly to avoid hypotension, bradycardia, arrythmias,
cardiac arrest
✓ a solution of 10% calcium gluconate with 1 liter of 5% dextrose in
water and administered as a slow IV bolus or a slow IV infusion
using a volumetric infusion pump
→ NURSING MANAGEMENT: assessment as severe hypocalcemia is life-
threatening, weight-bearing exercises to decrease bone calcium loss,
patient teaching related to diet and medications, and nursing care related
to IV calcium administration
give 30 minutes before meals and/or at bedtime for best absorption
Vitamin D given in conjunction with Calcium and for better GI
absorption
Patient with CRF must be prescribed with Aluminum hydroxide,
calcium acetate, or calcium carbonate antacids to decrease elevated
phosphorus levels before treating hypocalcemia
Increase dietary intake of calcium to at least 1,000 – 1,500 mg/day
*food sources: milk products; green, leafy vegetables; canned salmon;
sardines; fresh oysters
seizure precautions for severe hypocalcemia
monitor status of airway due to laryngeal stridor
instruct patient to have an adequate dietary calcium and consider
calcium supplements
a once-a-month biphosphonate drugs administered to reduce the rate
of bone loss
inform patients on the following risk factors:
➢ alcohol and caffeine inhibit calcium absorption
➢ cigarette smoking increases urinary excretion of calcium
➢ risk of falls
➢ avoid the overuse of laxatives and antacids
▪ HYPERCALCEMIA
→ Serum level above 10.5 mg/dL
→ ETIOLOGY:
Hyperparathyroidism and malignancies,
Movement of Ca from bones to serum (bone tumors; multiple myeloma)
Decreased renal excretion of Ca due to renal failure
Excessive administration/ingestion of Ca
Excessive intake of Vitamin D (↑Ca absorption)
Administration of thiazide diuretics (↓urinary Ca) excretion, Milk-alkali
syndrome
→ CLINICAL MANIFESTATIONS:
Hypercalciuria – Ca deposits in renal pelvis & parenchyma;
Lost of kidneys’ ability to concentrate urine; Flank pain; kidney
infection; kidney stones; polyuria; renal failure; Excessive thirst
Gastrointestinal disorders dt an increase Ca ions in sympathetic
ganglia (impedes transmission of stimuli) diarrhea, constipation, atony
of intestinal tract, peptic ulcer, anorexia, N/V; complicated with
abdominal distention & paralytic ileus
Behavioral changes due to neurologic hypofunction: lethargy;
exhaustion; mental confusion; slurred speech; loss of interest in
surroundings; coma serum Ca level at 16 mg/dL
Decalcification of bones (calcium moves from bones into blood):bone
pain; osteoporosis; osteomalacia; pathologic fractures
 Increased calcium in serum; increased renal Ca excretion; altered
cardiac muscle function – calcium levels above 11 mg/dl; definitive
ECG tracing; phosphorus often decreased; Sulcowitch test shows
increased Ca precipitation
Hypercalcemic crisis
→ DIAGNOSTIC FINDINGS:
serum Ca > 10.2 mg/dL
dysrythmias; shortening of the QT interval; prolonged PR interval
PTH increased in hyperparathyroidism and suppressed in malignancy
X-ray reveals osteoporosis
Dense precipitation due to hypercalciuria
→ NURSING DIAGNOSES:
Knowledge deficit regarding excessive ingestion of Ca and Vit. D
Knowledge deficit regarding need for hydration and weight bearing
activity when vulnerable to Ca excess
Altered urinary elimination patterns r/t hypercalciuria
Risk for injury due to mental confusion
Risk for injury due to fractures arising from loss of Ca from the bone
matrix
Impaired in bowel elimination: constipation or diarrhea
→ MEDICAL MANAGEMENT:
treat underlying cause, administer fluids, furosemide, phosphates,
calcitonin, and biphosphonates
To promote Ca excretion:
➢ ensure adequate hydration using saline solutions(inhibit tubular
reabsorption of Ca)
➢ use phosphate supplements- enhance Ca deposits in bone and soft
tissue; to reduce absorption of intestinal Ca(administered orally or
in NGT- Phospho-soda; Neutra-phos)
➢ employ glucocorticoids- ↓ absorption from GIT & reabsorption of
tubular Ca
➢ administer mithramycin, used for hypercalcemia due to malignancy
(used to treat testicular neoplasm; causes thrombocytopenia; renal
and hepatic damage)
➢ administer calcitonin - lower Ca levels due to excessive parathyroid
activity; by IM (has a risk of anaphylaxis; keep epinephrine,
antihistamines, and O2 on hand; useful for those with heart disease
and renal failure)
→ TO PREVENT HYPERCALCEMIA:
encourage early and regular ambulation  ensuring adequate hydration
and diuresis
inform people taking vitamins that overdose of Calcium and vitamin D
can cause Ca excess
→ NURSING MANAGEMENT:
assessment as hypercalcemic crisis; fluids of 3 to 4 L/d, provide fluids
containing sodium unless contraindicated and fiber for constipation,
and ensure safety
Inform patient the importance of frequent ambulation.
Fluids containing sodium should be administered unless
contraindicated; favors Ca excretion.
Patients are encouraged to drink 3- 4 quarts of fluid daily.
Adequate fiber diet.
Inform patient and family that mental changes are reversible with
treatment.
Assess patient s/s for digitalis toxicity.
Cardiac rate and rhythm are monitored for any abnormalities
• MAGNESIUM: hypomagnesemia and hypermagnesemia
- Magnesium (1.3-2.3 meq/L or 1.8- 3mg/dl)
- Most abundant intracellular cation after potassium
- Functions of Magnesium: neuromuscular function, CV effects: Vasodilation & ↓
peripheral resistance
- Ingestion of Mg++ requires 200-300 mg/day
- Absorption of Mg++ is only 45 %
- Excretion in the feces
- Inhibit the release of Acetylcholine
- Similar with Calcium
▪ HYPOMAGNESEMIA
→ Serum level less than 1.8 mg/dL; evaluate in conjunction with serum
albumin
→ CAUSES: alcoholism, GI losses, enteral or parenteral feeding deficient
in Mg, meds:(Aminoglycosides, diuretics, digitalis); rapid administration
of citrated blood;
→ MANIFESTATIONS: neuromuscular irritability, muscle weakness,
tremors, athetoid movements (slow, involuntary twisting & writhing)
ECG changes and dysrhythmias, and alterations in mood and level of
consciousness
→ MEDICAL MANAGEMENT: diet, oral magnesium, and magnesium
sulfate IV
→ NURSING MANAGEMENT: assessment, ensure safety, patient
teaching related to diet, medications, alcohol use, and nursing care
related to IV magnesium sulfate
Hypomagnesemia is often accompanied by hypocalcemia
Monitor and treat potential hypocalcemia
Dysphagia is common in magnesium-depleted patients; assess
ability to swallow with water before administering food or
medications
▪ HYPERMAGNESEMIA
→ Serum level more than 2.7 mg/dL
→ CAUSES: renal failure, diabetic ketoacidosis, and excessive
administration of magnesium
→ MANIFESTATIONS: flushing, lowered BP, nausea, vomiting,
hypoactive reflexes, drowsiness, muscle weakness, depressed
respirations, ECG changes, and dysrhythmias
→ MEDICAL MANAGEMENT: IV calcium gluconate, loop diuretics, IV
NS of RL, hemodialysis
→ NURSING MANAGEMENT: assessment, avoid administering
medications containing magnesium, and provide patient teaching
regarding magnesium-containing OTC medications
• PHOSPHORUS: hypophosphatemia and hyperphosphatemia
▪ HYPOPHOSPHATEMIA
→ Serum level below 2.5 mg/dL
→ CAUSES: alcoholism, refeeding of patients after starvation, pain,
heat stroke, respiratory alkalosis, hyperventilation, diabetic
ketoacidosis, hepatic encephalopathy, major burns,
hyperparathyroidism, low magnesium, low potassium, diarrhea,
vitamin D deficiency, and diuretic and antacid use
→ MANIFESTATIONS: neurologic symptoms, confusion, muscle
weakness, tissue hypoxia, muscle and bone pain, and increased
susceptibility to infection
→ MEDICAL MANAGEMENT: oral or IV phosphorus replacement
→ NURSING MANAGEMENT: assessment, encourage foods high in
phosphorus, and gradually introduce calories for malnourished
patients receiving parenteral nutrition
▪ HYPERPHOSPHATEMIA
→ Serum level above 4.5 mg/dL
→ CAUSES: renal failure, excess phosphorus, excess vitamin D,
acidosis, hypoparathyroidism, and chemotherapy
→ MANIFESTATIONS: few symptoms, soft-tissue calcifications,
symptoms occur due to associated hypocalcemia
→ MEDICAL MANAGEMENT: treat underlying disorder; use vitamin D
preparations, calcium-binding antacids, phosphate-binding gels or
antacids, loop diuretics, NS IV, and dialysis
→ NURSING MANAGEMENT: assessment, avoid high-phosphorus
foods, and provide patient teaching related to diet, phosphate
containing substances, and signs of hypocalcemia
• CHLORIDE: hypochloremia and hyperchloremia
▪ HYPOCHLOREMIA
→ Serum level less than 96 mEq/L
→ CAUSES: Addison’s disease, reduced chloride intake, GI loss,
diabetic ketoacidosis, excessive sweating, fever, burns, medications,
and metabolic alkalosis
Loss of chloride occurs with loss of other electrolytes, potassium,
and sodium
→ MANIFESTATIONS: agitation, irritability, weakness, hyperexcitability
of muscles, dysrhythmias, seizures, and coma
→ MEDICAL MANAGEMENT: replace chloride—IV, NS, or 0.45% NS
→ NURSING MANAGEMENT: assessment, avoid free water,
encourage high-chloride foods, and provide patient teaching related
to high-chloride foods
▪ HYPERCHLOREMIA
→ Serum level more than 108 mEq/L
→ CAUSES: excess sodium chloride infusions with water loss, head
injury, hypernatremia, dehydration, severe diarrhea, respiratory
alkalosis, metabolic acidosis, hyperparathyroidism, and medications
→ MANIFESTATIONS: tachypnea, lethargy, weakness, rapid, deep
respirations, hypertension, and cognitive changes
→ MEDICAL MANAGEMENT: restore electrolyte and fluid balance,
LR, sodium bicarbonate, and diuretics
→ NURSING MANAGEMENT: assessment, provide patient teaching
related to diet and hydration
MAINTAINING ACID–BASE BALANCE:
• Normal plasma pH is 7.35 to 7.45: hydrogen ion concentration
• Major extracellular fluid buffer system; bicarbonate-carbonic acid buffer system
• Kidneys regulate bicarbonate in ECF
• Lungs under the control of the medulla regulate CO2 and, therefore, carbonic
acid in ECF
• Other buffer systems
▪ ECF: inorganic phosphates and plasma proteins
▪ ICF: proteins, organic and inorganic phosphates
▪ Hemoglobin
METABOLIC ACIDOSIS:
• Low pH <7.35
• Low bicarbonate <22 mEq/L
• MANIFESTATIONS: headache, confusion, drowsiness, increased respiratory
rate and depth, decreased blood pressure, decreased cardiac output,
dysrhythmias, shock; if decrease is slow, patient may be asymptomatic until
bicarbonate is 15 mEq/L or less
• Correct the underlying problem and correct the imbalance; bicarbonate may be
administered
• With acidosis, hyperkalemia may occur as potassium shifts out of the cell
• As acidosis is corrected, potassium shifts back into the cell and potassium
levels decrease
• Monitor potassium levels  Serum calcium levels may be low with chronic
metabolic acidosis and must be corrected before treating the acidosis
METABOLIC ALKALOSIS:
• High pH >7.45
• High bicarbonate >26 mEq/L
• Most commonly due to vomiting or gastric suction; may also be caused by
medications, especially long-term diuretic use
• Hypokalemia will produce alkalosis
• MANIFESTATIONS: symptoms related to decreased calcium, respiratory
depression, tachycardia, and symptoms of hypokalemia
• Correct underlying disorder, supply chloride to allow excretion of excess
bicarbonate, and restore fluid volume with sodium chloride solutions
 RESPIRATORY ACIDOSIS:

• Low pH 42 mm Hg
• Always due to a respiratory problem with inadequate excretion of CO2
• With chronic respiratory acidosis, the body may compensate and may be
asymptomatic; symptoms may include a suddenly increased pulse, respiratory
rate, and BP; mental changes; feeling of fullness in the head
• Potential increased intracranial pressure
• Treatment is aimed at improving ventilation

RESPIRATORY ALKALOSIS:

• High pH >7.45
• PaCO2 <35 mmHg
• Always due to hyperventilation
• MANIFESTATIONS: lightheadedness, inability to concentrate, numbness and
tingling, and sometimes loss of consciousness
• Correct cause of hyperventilation

ARTERIAL BLOOD GASES:

• pH 7.35 (7.4) to 7.45

• PaCO2 35 (40) to 45 mm Hg
• HCO3 ˉ 22 (24) to 26 mEq/L (assumed average values for ABG interpretation)
• PaO2 80 to 100 mm Hg
• Oxygen saturation >94%
• Base excess/deficit ±2 mEq/L COMPLICATIONS OF IV THERAPY:

• Fluid overload
• Air embolism
• Septicemia and other infections
• Infiltration and extravasation
• Phlebitis
• Thrombophlebitis
• Hematoma
• Clotting and obstruction