Acute Biologic Crisis

ICU Nursing
Rachelle M. Ganuelas, RN, MAN

Burns
Definition: Cellular destruction of the layers of the skin and the resultant depletion of fluids
and electrolytes. These are skin injuries resulting from various injurious factors.

Burns

Burn injuries depend on:

History of the injury

Causative factor

Temperature of the burning agent

Duration of contact with the agent

Thickness of the skin

Types of Burns according to ETIOLOGY

1. Thermal: most common type; caused by flame, flash, scalding, and contact (hot metals, grease)

Types of Burns according to ETIOLOGY

2. Smoke inhalation: occurs when smoke (particulate products of a fire, gases, and superheated air)
causes respiratory tissue damage

Types of Burns according to ETIOLOGY

3. Chemical: caused by tissue contact, ingestion or inhalation of acids, alkalies, or vesicants

Types of Burns according to ETIOLOGY

4. Electrical: injury occurs from direct damage to nerves and vessels when an electric current passes
through the body.

Types of Burns according to ETIOLOGY

5. Radiation Burns- This is caused by exposure to ultraviolet rays, x-rays and radioactive sources.

SKIN
 Largest organ of the body

Functions:

 Protection

 Sensation

 Fluid balance

 Temperature regulation

 Vitamin D production

 Immune response

Burn classification as to depth

Superficial Partial thickness

(1st degree)

Outer layer of dermis

Erythema, pain up to 48 hrs

Healing 1-2 wks [sunburn]

Burn classification as to depth

Deep Partial thickness

(2nd degree)

Epidermis & dermis involved

Blisters & edema, frequently quite painful

Healing 14-21 days

Burn classification as to depth

Full thickness (3rd degree)

Epidermis, dermis, subcutaneous fat are involved

Dry, pearly white or charred in appearance

Not painful
 Eschar must be removed; may need grafting

ESTIMATION of BURNS

Various methods are utilized for estimating the extent of burn injury

1. The Rule of Nines in adults

Head and Neck- 9%

Anterior trunk- 18%

Posterior trunk- 18%

Upper arms- 18% ( 9% each x 2)

Lower ext- 36% ( 18% EACH X 2)

Perineum- 1%

Burn estimation

2. LUND AND BROWDER or BERKOW method

Modifies percentages for body segments according to age

Provides a more accurate estimate of the burn size

Uses a diagram of the body divided into sections, with the representative % of TBSA for all
ages

Lund-Browder Chart

PATHOPHYSIOLOGY OF BURNS

Burns are caused by transfer of energy from a heat source to the body

Tissue destruction results from COAGULATION, Protein denaturation, or Ionization of cellular

contents from a thermal, radiation or chemical source.

PATHOPHYSIOLOGY OF BURNS

Following burns, Vasoactive substances are released from the injured tissue and these
substances cause an increase in the capillary permeability allowing the plasma to seep to the
surrounding tissues

PATHOPHYSIOLOGY OF BURNS
 The generalized edema, evaporation of fluids and capillary membrane permeability result to
DECREASED circulating blood volume

PATHOPHYSIOLOGY OF BURNS

The decrease in blood volume results to decrease organ perfusion

The blood volume decreases, BP and Cardiac output decrease and the body compensates by
increasing heart rate

The hematocrit level increases as a result of plasma loss

PATHOPHYSIOLOGY OF BURNS

The body mobilizes compensatory mechanisms- blood is shunted from the kidney, skin and
GIT to the BRAIN. Oliguria is expected, as well as intestinal ileus and GI dysfunction

The immune system is depressed, resulting in immunosuppression and increased risk for
infection

PATHOPHYSIOLOGY OF BURNS

The pulmonary system may react by pulmonary vasoconstriction causing a decreased oxygen
tension and pulmonary hypertension

Tissue destruction initially causes HYPERKALEMIA because injured tissues release K+

HYPONATREMIA may be expected because of PLASMA LOSS (with Na+) into the interstitial
space

Assessment Findings

Superficial Partial Thickness Burns (1st)

 Local erythema

 No Blister formation

 Mild local pain

 Rapid healing WITHOUT scarring

Assessment Findings

Deep Partial Thickness (2ND)

Tissue destruction of epidermis-dermis

Skin appears red to ivory, moist

 Wet, large and thin blisters

Intact tactile and pain sensation, moderate to severe pain

Healing is variable and with scarring

Assessment Findings

Full Thickness Burns (THIRD DEGREE)

Injury appears WHITE, or black, with thrombosed veins

Dry, leathery appearance due to loss of epidermal elasticity

Marked EDEMA

Painless to touch due to destruction of superficial nerves

Burn Management

1.EMERGENT PHASE

Begins at the time of injury and ends with the restoration of the capillary permeability ( with
48-72 hours)

The GOAL is to PREVENT hypovolemic shock and preserve the vital body organ function

Emergency and pre-hospital care

Burn Management

2.RESUSCITATIVE PHASE

Begins with the initiation of fluids and ENDS when capillary integrity returns to near-normal
and large fluid shifts have decreased

The GOAL is to prevent shock by maintaining adequate circulating blood volume to maintain
vital organ perfusion

Burn Management

3.ACUTE PHASE

Begins when the client is HEMODYNAMICALLY stable, capillary permeability is restored and
DIURESIS has begun

Emphasis is placed on restorative therapy and the phase continues until wound closure is
achieved
 The FOCUS is on infection control, wound care, wound closure, nutritional support, pain
management and physical therapy

Burn Management

4.REHABILITATIVE PHASE

The final phase of Burn care, restoration of functions, cosmetic surgery

Goals of this phase – patient independence and restoration of maximal function

Medical Management

Medical management

1. Supportive therapy: fluid management (lVFs), catheterization

2. Wound care: hydrotherapy, debridement (enzymatic or surgical)

Medical Management

3. Drug therapy

a. Topical antibiotics: mafenide (Sulfamylon), silver sulfadiazine (Silvadene), silver nitrate,

povidone-iodine (Betadine) solution

b. Systemic antibiotics: gentamicin

c. Tetanus toxoid or hyperimmune human tetanus globulin (burn wound good medium for
anaerobic growth)

d. Analgesics

4. Surgery: excision and grafting

Nursing Management

1. Emergent phase (time of injury)

Remove person from source of burn.

1) Thermal: smother burn beginning with the head.

2) Smoke inhalation: ensure patent airway.

3) Chemical: remove clothing that contains chemical; lavage area with copious amounts of
water.

4) Electrical: note victim position, identify entry/exit routes, maintain airway.

 Nursing Management

1. Emergent phase (time of injury)

Cool the burn for several minutes. DON’T USE ICE!!

Wrap in dry, clean sheet or blanket to prevent further contamination of wound and provide
warmth and conserve body heat.

Assess how and when burn occurred.

Nursing Management

1. Emergent phase (time of injury)

Remove constricting clothes and jewelry

Cover the wound with a sterile dressing or clean, dry cloth

Provide IV route only if possible

Transport immediately to a hospital or burn facility

Nursing Management

2. Resuscitative and Shock phase (first 24—48 hours)

Provide appropriate fluid resuscitation based on the Parkland formula

4 mL Plain LR x %TBSA of burns x kg body weight

Nursing Management

3. Fluid remobilization or diuretic phase (2—5 days post burn)

Monitor and treat potential complications like acute renal failure, paralytic ileus, Curling’s
ulcer and hypokalemia

Nursing Management

4. Convalescent phase

a. Starts when diuresis is completed and wound healing and coverage begin.

GENERAL NURSING INTERVENTIONS IN THE HOSPITAL

1. Provide relief/control of pain.

a. Administer morphine sulfate IV and monitor vital signs closely.

 b. Administer analgesics/narcotics 30 minutes before wound care.

c. Position burned areas in proper alignment

GENERAL NURSING INTERVENTIONS IN THE HOSPITAL

2. Monitor alterations in fluid and electrolyte balance.

a. Assess for fluid shifts and electrolyte alterations

b. Monitor Foley catheter output hourly (30 cc per hour desired).

c. Weigh daily.

d. Monitor circulation status regularly.

e. Administer/monitor crystálloids/colloids

GENERAL NURSING INTERVENTIONS IN THE HOSPITAL

3. Promote maximal nutritional status.

a. Monitor tube feedings if Peripheral Nutrition is ordered.

NPO immediately after injury!!! ONLY when oral intake permitted, provide high-calorie, high-
protein, high- carbohydrate diet with vitamin and mineral supplements.

c. Serve small portions.

d. Schedule wound care and other treatments at least 1 hour before meals.

GENERAL NURSING INTERVENTIONS IN THE HOSPITAL

4. Prevent wound infection.

a. Place client in controlled sterile environment.

b. Use hydrotherapy for no more than 30 minutes to prevent electrolyte loss.

Observe wound for separation of eschar and cellulitis.

GENERAL NURSING INTERVENTIONS IN THE HOSPITAL

5. Prevent GI complications.

a. Assess for signs and symptoms of paralytic ileus.

b. Assist with insertion of NG tube to prevent/control Curling’s/stress ulcer; monitor

patency/drainage.
 GENERAL NURSING INTERVENTIONS IN THE HOSPITAL

5. Prevent GI complications.

c. Administer prophylactic antacids through NG tube and/or IV cimetidine (Tagamet) or

ranitidine (Zantac) (to prevent stress ulcer).

d. Monitor bowel sounds.

e. Test stools for occult blood.

Rehabilitation

Methods of coping and re-socialization

Ensure optimum nutrition

Initiate physical therapy to regain and maintain optimal range of motion and achieve wound
coverage

Provide psychosocial support to promote mental health

Rehabilitation

Provide family-centered care to promote integrity of the family as a unit

Encourage post-discharge follow-up for several years

Ensure appropriate referral to cosmetic surgeon, psychiatrist, occupational therapist,

nutritionist and physical therapist

Drugs for Burns

Mafenide (Sulfamylon)

1) Administer analgesics 30 minutes before application.

2) Monitor acid-base status and renal function studies. SIDE EFFECT: LACTIC ACIDOSIS

3) Provide daily BATH for removal of previously applied cream.

Drugs for Burns

Silver sulfadiazine (Silvadene)

1) Administer analgesics 30 minutes before application.

2) Observe for and report hypersensitivity reactions (rash, itching, burning sensation in
unburned areas).
 3) Store drug away from heat

Drugs for Burns

Silver nitrate

1) Handle carefully; solution leaves a gray or black stain on skin, clothing, and utensils.

2) Administer analgesic before application.

3) Keep dressings wet with solution; dryness increases the concentration and causes
precipitation of silver salts in the wound.

Drugs for Burns

Povidone-iodine (Betadine)

Administer analgesics before application.

Assess for metabolic acidosis/renal function

Gentamicin

Assess vestibular/auditory and renal functions at regular intervals.

Cimetidine

Given to prevent Curling’s ulcer

Acute Myocardial Infarction

Myocardial infarction

Death of myocardial tissue in regions of the heart with abrupt interruption of coronary blood
supply

Myocardial infarction

ETIOLOGY and Risk factors

1. CAD

2. Coronary vasospasm

3. Coronary artery occlusion by embolus and thrombus

4. Conditions that decrease perfusion- hemorrhage, shock

 Myocardial infarction

Risk factors

1. Hypercholesterolemia

2. Smoking

3. Hypertension

4. Obesity

5. Stress

6. Sedentary lifestyle

Myocardial infarction

PATHOPHYSIOLOGY

Interrupted coronary blood flowà myocardial ischemia àanaerobic myocardial metabolism for
several hoursà myocardial death à depressed cardiac function à triggers autonomic nervous
system response à further imbalance of myocardial O2 demand and supply

Myocardial infarction

ASSESSMENT findings

1. CHEST PAIN

Chest pain is described as severe, persistent, crushing substernal discomfort

Radiates to the neck, arm, jaw and back

Myocardial infarction

ASSESSMENT findings

1. CHEST PAIN

Occurs without cause, primarily early morning

NOT relieved by rest or nitroglycerin

Lasts 30 minutes or longer

Signs and symptoms

Chest pain – major symptom

P- provoked: during exertion or rest

Myocardial infarction

Assessment findings

2. Dyspnea

3. Diaphoresis

4. cold clammy skin

5. N/V

6. restlessness, sense of doom

7. tachycardia or bradycardia

8. hypotension

9. S3 and dysrhythmias

Myocardial infarction

Laboratory findings

1. ECG- the ST segment is ELEVATED. T wave inversion, presence of Q wave

2. Myocardial enzymes- elevated CK-MB, LDH and Troponin levels

3. CBC- may show elevated WBC count

4. Test after the acute stage- Exercise tolerance test, thallium scans, cardiac catheterization

The Cardiovascular System

LABORATORY PROCEDURES

CARDIAC catheterization

Insertion of a catheter into the heart and surrounding vessels

Determines the structure and performance of the heart valves and surrounding vessels

The Cardiovascular System

LABORATORY PROCEDURES

CARDIAC catheterization
Used to diagnose CAD, assess coronary atery patency and determine extent of atherosclerosis

The Cardiovascular System

LABORATORY PROCEDURES

Pretest: Ensure Consent, assess for allergy to seafood and iodine, NPO, document weight and
height, baseline VS, blood tests and document the peripheral pulses

The Cardiovascular System

LABORATORY PROCEDURES

Pretest: Fast for 8-12 hours, teachings, medications to allay anxiety

The Cardiovascular System

LABORATORY PROCEDURES

Intra-test: inform patient of a fluttery feeling as the catheter passes through the heart; inform
the patient that a feeling of warmth and metallic taste may occur when dye is administered

The Cardiovascular System

LABORATORY PROCEDURES

Post-test: Monitor VS and cardiac rhythm

Monitor peripheral pulses, color and warmth and sensation of the extremity distal to insertion
site

Maintain sandbag to the insertion site if required to maintain pressure

Monitor for bleeding and hematoma formation

The Cardiovascular System

LABORATORY PROCEDURES

Maintain strict bed rest for 6-12 hours

Client may turn from side to side but bed should not be elevated more than 30 degrees and
legs always straight

Encourage fluid intake to flush out the dye

Immobilize the arm if the antecubital vein is used

Monitor for dye allergy

Myocardial infarction

Nursing Interventions
1. Provide Oxygen at 2 lpm, Semi-fowler’s

2. Administer medications

 Morphine to relieve pain

 nitrates, thrombolytics, aspirin and anticoagulants

 Stool softener and hypolipidemics

3. Minimize patient anxiety

 Provide information as to procedures and drug therapy

Myocardial infarction

4. Provide adequate rest periods

5. Minimize metabolic demands

 Provide soft diet

 Provide a low-sodium, low cholesterol and low fat diet

6. Minimize anxiety

 Reassure client and provide information as needed

Myocardial infarction

7. Assist in treatment modalities such as PTCA and CABG

8. Monitor for complications of MI- especially dysrhythmias, since ventricular tachycardia can happen
in the first few hours after MI

9. Provide client teaching

PTCA

PERCUTANEOUS TRANSLUMINAL CORONARY ANGIOPLASTY (PTCA)

A. General information:

1. PTCA can be performed instead of coronary artery bypass graft surgery in various clients with
single vessel CAD.

2. Aim: revascularize the myocardium

decrease angina – increase survival

 3. a balloon tipped catheter is inserted into the stenotic, diseased coronary artery. The balloon is
inflated with a controlled pressure and thereby decreases the stenosis of the vessel

CORONARY ARTERY BYPASS SURGERY

A. General information:

1. A coronary artery bypass graft is the surgery of choice for clients with severe CAD

2. new supply of blood brought to diseased/occluded coronary artery by bypassing the

obstruction with a graft that is attached to the aorta proximally and to the coronary artery distally

3. Procedure requires use of extracorporeal circulation (heart-lung machine, cardiopulmonary

bypass)

CORONARY ARTERY BYPASS SURGERY

B. Nursing interventions: preoperative

1. Explain anatomy of the heart, function of coronary arteries, effects of CAD

2. Explain events of the day of surgery

3. Orient to the critical and coronary care units and introduce to staff

4. Explain equipments to be used (monitors, hemodynamic procedures, ventilators, ET, etc)

5. Demonstrate activity and exercise

6. Reassure availability of pain medications

CORONARY ARTERY BYPASS SURGERY

C. Nursing interventions: post-operative

1. Maintain patent airway

2. Promote lung re-expansion

3. monitor cardiac status

4. maintain fluid and electrolyte balance

5. maintain adequate cerebral circulation

6. provide pain relief

7. prevent abdominal distension

CORONARY ARTERY BYPASS SURGERY

8. Monitor for and prevent the ff. complications:

a. Thrombophlebitis / pulmonary embolism

b. Cardiac tamponade

c. arrhythmias

d. CHF

9. Provide client teaching and discharge planning concerning:

a. limitation with progressive increase in activities

CORONARY ARTERY BYPASS SURGERY

b. sexual intercourse can usually be resumed by 3 rd or 4th week post-op

c. medical regimen

d. meal planning with prescribed modifications

e. wound cleansing daily with mild soap and H2O and report for any signs of infection

f. Symptoms to be reported:

- fever, dyspnea, chest pain with minimal exertion

MI

Medical Management

1. ANALGESIC

 The choice is MORPHINE

 It reduces pain and anxiety

 Relaxes bronchioles to enhance oxygenation

MI

Medical Management

2. ACE

 Prevents formation of angiotensin II

 Limits the area of infarction

 MI

Medical Management

3. Thrombolytics

 Streptokinase, Alteplase

 Dissolve clots in the coronary artery allowing blood to flow

Myocardial infarction

NURSING INTERVENTIONS AFTER ACUTE EPISODE

1. Maintain bed rest for the first 3 days

2. Provide passive ROM exercises

3. Progress with dangling of the feet at side of bed

Myocardial infarction

NURSING INTERVENTIONS AFTER ACUTE EPISODE

4. Proceed with sitting out of bed, on the chair for 30 minutes TID

5. Proceed with ambulation in the roomà toiletà hallway TID

Myocardial infarction

NURSING INTERVENTIONS AFTER ACUTE EPISODE

Cardiac rehabilitation

To extend and improve quality of life

Physical conditioning

Patients who are able to walk 3-4 mph are usually ready to resume sexual activities

Medical and nursing management

Major goals of care:

1. Treatment of acute attack

2. Prevent life-threatening complications

3. Rehabilitation
 Treatment of acute attack

Administer oxygen

Semi – fowler’s position

Treatment of acute attack

Thrombolytic agents

- given 3-12 hrs after onset

- Streptokinase, urokinase, tissue- type plasminogen activator (TPA)

Aspirin

Treatment of acute attack

ECG monitoring

- dysrhythmias

Treatment of acute attack

Mild laxatives

Monitor vital signs

Diet

- clear liquid diet for 24-48 hrs then small and soft meals, low Na diet

- no iced or very hot drinks

Prevent life-threatening complications

Arrhythmias

Shock

Heart failure and pulmonary edema

Pulmonary Embolism

Rehabilitation

Goal: to live a full, vital and productive life

Gradually increase activity

 Stop smoking completely

Weight reduction

Exercise (walking, jogging, swimming)

The Cardiovascular System

LABORATORY PROCEDURES

CVP

The CVP is the pressure within the SVC

Reflects the pressure under which blood is returned to the SVC and right atrium

The Cardiovascular System

LABORATORY PROCEDURES

CVP

Normal CVP is 0 to 8 mmHg/ 4-10 cm H2O

Elevated CVP indicates increase in blood volume, excessive IVF or heart/renal failure

Low CVP may indicated hypovolemia, hemorrhage and severe vasodilatation

The Cardiovascular System

LABORATORY PROCEDURES

Measuring CVP

1. Position the client supine with bed elevated at 45 degrees

2. Position the zero point of the CVP line at the level of the right atrium. Usually this is at the
MAL, 4th ICS

3. Instruct the client to be relaxed and avoid coughing and straining.

Electrical System of the Heart

Dysrhythmias

• Dysrhythmias: disorders of the formation or conduction (or both) of the electrical impulses in
the heart

• These disorders can cause disturbances of:

– Rate
 – Rhythm

– Both rate and rhythm

• Potentially can alter blood flow & cause hemodynamic changes

• Diagnosed by analysis of ECG waveform

DYSRHYTHMIAS

An arrhythmia is a disruption in the normal events of the cardiac cycle. It may take a variety of
forms.

Treatment varies on the type dysrhythmias

SINUS TACHYCARDIA

A. General Information:

1. A heart rate of over 100 beats/min, originating in the SA node

DYSRHYTHMIAS

2. May be caused by:

- fever - anemia

- apprehension - hyperthyroidism

- physical activity - myocardial ischemia

- caffeine - drugs (epi., theo)

B. Assessment findings:

1. Rate: 100-160 beats /min

2. Rhythm: regular

DYSRHYTHMIAS

3. P wave: precedes each QRS complex with normal contour

4. P-R interval: normal (0.08 sec)

5. QRS complex: normal (0.06 sec)

C. Treatment;

- correction of underlying cause, elimination of stimulants, sedatives, propranolol (Inderal)

 Sinus Tachycardia

DYSRHYTHMIAS

SINUS BRADYCARDIA

A. General Information:

1. A slowed heart rate initiated by SA node

2. Caused by:

- excessive vagal or decreased sympathetic tone

- MI - IC tumors

- meningitis - myxedema

- cardiac fibrosis

- normal variation of the heart rate in well trained athletes

DYSRHYTHMIAS

B. Assessment findings:

1. Rate: <60 beats/min

2. Rhythm: regular

3. P wave: precedes each QRS with a normal contour

4. P-R interval: normal

5. QRS complex: normal

C. Treatment: usually not needed

- if cardiac output is inadequate: atropine and isoproterenol; pacemaker

Sinus Bradycardia

DYSRHYTHMIAS

ATRIAL FIBRILLATION

A. General information

1. An arrhythmia in which ectopic foci cause rapid, irregular contractions of the heart
 2. seen in clients with

- rheumatic mitral stenosis - thyrotoxicosis

- cardiomyopathy - pericarditis

- hypertensive heart disease - CHD

DYSRHYTHMIAS

B. Assessment findings:

1. Rate: atrial: 350-600 beats/min

ventricular: varies bet. 100-160 beats /min

2. Rhythm: atrial and ventricular regularly irregular

3. P wave: no definite P wave; rapid undulations called fibrillatory waves

4. P-R interval: not measurable

5. QRS complex: generally normal

ATRIAL FIBRILLATION

DYSRHYTHMIAS

C. Treatment: digitalis preparations, propanolol, verapamil in conjunction with digitalis; direct current
cardioversion

PREMATURE VENTRICULAR CONTRACTIONS

A. General Information:

1. Irritable impulses originate in the ventricles

2. Caused by:

- electrolyte imbalance (hypokalemia)

- digitalis drug therapy

Premature Ventricular Contraction (PVC)

DYSRHYTHMIAS

Cont’d: (causes)

- stimulants( caffeine, epinephrine, isoproterenol)

 - hypoxia

- CHF

B. Assessment findings:

1. Rate: varies according to no. of PVC’s

2. Rhythm: irregular because of PVC’s

3. P wave: normal; however, often lost in QRS complex

DYSRHYTHMIAS

4. P-R interval: often not measurable

5. QRS complex: greater then 0.12secs, wide

C. Treatment:

1. IV push of Lidocaine (50-100mg) followed by IV drip of lidocaine at rate of 1-4 mg/min

2. Procainamide, quinidine

3. Treatment of underlying cause

DYSRHYTHMIAS

VENTRICULAR TACHYCARDIA

A. General information:

1. 3 or more consecutive PVC’s; occurs from repetitive firing of an ectopic focus in the ventricles

2. caused by:

- MI - CAD

- digitalis intoxication - hypokalemia

Ventricular Tachycardia

DYSRHYTHMIAS

B. Assessment findings:

1. Rate: atrial: 60-100 beats/min

ventricular: 110-250 beats/min

 2. Rhythm: atrial(regular), ventricular (occly. irregular)

3. P wave: often lost in QRS complex

4. P-R interval usually not measurable

5. QRS complex: greater than 0.12 secs, wide

DYSRHYTHMIAS

C. Treatment:

1. IV push of lidocaine (50-100mg), then IV drip of lidocaine 1-4 mg/min

2. Procainamide via IV infusion of 2-6 mg/min

3. direct current cardioversion

4. bretylium, propanolol

Nursing Process: The Care of the Patient with a Dysrhythmia: Assessment

• Assess indicators of cardiac output and oxygenation, especially changes in level of

consciousness.

• Physical assessment includes:

– Rate and rhythm of apical and peripheral pulses

– Assess heart sounds

– Blood pressure and pulse pressure

– Signs of fluid retention

• Health history: include presence of coexisting conditions and indications of previous occurrence

• Medications

Nursing Process: The Care of the Patient with a Dysrhythmia: Diagnosis

Decreased cardiac output

Anxiety

Deficient knowledge

Collaborative Problems/Potential Complications

Cardiac arrest
Heart failure

Thromboembolic event, especially with atrial fibrillation

Nursing Process: The Care of the Patient with a Dysrhythmia: Planning

Goals may include eradicating or decreasing the occurrence of the dysrhythmia to maintain
cardiac output, minimizing anxiety, and acquiring knowledge about the dysrhythmia and its
treatment.

Decreased Cardiac Output

Monitoring

 ECG monitoring

 Assessment of signs and symptoms

Administration of medications and assessment of medication effects

Adjunct therapy: cardioversion, defibrillation, pacemakers

Other Interventions

Anxiety

 Use a calm, reassuring manner.

 Measures to maximize patient control to make episodes less threatening

 Communication and teaching

Teaching self-care

 Include family in teaching

Pacemakers

An electronic device that provides electrical stimuli to the heart muscle

Types:

 Permanent

 Temporary

Implanted Transvenous Pacemaker

Transcutaneous Pacemaker
 ECG On-Demand Pacing

Complications of Pacemaker Use

Infection

Bleeding or hematoma formation

Dislocation of the lead

Skeletal muscle or phrenic nerve stimulation

Cardiac tamponade

Pacemaker malfunction

Phrenic nerve

Nursing Process: The Care of the Patient with an Implanted Cardiac Device: Assessment

Device function; ECG

Cardiac output and hemodynamic stability

Incision site

Coping

Patient and family knowledge

Nursing Process: The Care of the Patient with an Implanted Cardiac Device: Diagnosis

Risk for infection

Risk for ineffective coping

Knowledge deficiency

Nursing Process: The Care of the Patient with an Implanted Cardiac Device- Planning

Goals include absence of infection, adherence to self-care program, effective coping, and
maintenance of device function.

Interventions

• Risk for ineffective coping

– Support of patient and family coping

 – Setting of realistic goals

– Allow patient to talk, share feeling and experiences

– Support groups or referral

– Stress reduction techniques

• Knowledge deficiency

– Patient and family teaching

Cardioversion and Defibrillation

• Treat tachydysrhythmias by delivering an electrical current that depolarizes a critical mass of

myocardial ceils. When cells repolarize, the sinus node is usually able to recapture its role as
heart pacemaker.

• In cardioversion, the current delivery is synchronized with the patient’s ECG.

• In defibrillation, the current delivery is unsynchronized.

Safety Measures

Ensure good contact between skin and pads or paddles. Use a conductive medium and 20-25
pounds of pressure.

Place paddles so that they do not touch bedding or clothing and are not near medication
patches or oxygen flow.

If cardioverting, turn the synchronizer on.

If defibrillating, turn the synchronizer off.

Do not charge the device until ready to shock.

Call “clear” three times; follow checks required for clear and ensure that no one is in contact
with the patient, bed, or equipment.

Paddle Placement for Defibrillation

Implantable Cardioverter Defibrillator (ICD)

A device that detects and terminates life-threatening episodes of tachycardia or fibrillation

Antitachycardia pacing

ICD
 Invasive Methods to Diagnose and Treat Recurrent Dysrhythmias

Electrophysiologic studies

Cardiac conduction surgery

 Maze procedure

 Catheter ablation therapy

Cardioversion

Defibrillator Placement

CARDIAC ARREST

Sudden, unexpected cessation of breathing and adequate circulation of blood by the heart

Medical Management

1. Cardiopulmonary resuscitation (CPR)

2. DRUG THERAPY

EPINEPHRINE

enhance myocardial automaticity, excitability, conductivity and contractility

LIDOCAINE-mech of action: decrease cardiac excitability, cardiac conduction is delayed in the atrium and
ventricle

Administered via IV. Have dopamine available for circulatory depression

dosage: initial- 1 – 1.5mg/kg

infusion: 2 – 4mg/min

. Atropine (anticholinergic)-mech of action: blocks cholinergic receptor sites so response to acetylcholine

is decreased

dosage: 0.5 to 1mg IV, may repeat every 5 min for a total of 2-3mg

Dopamine (adrenergic)

mech of action: increased myocardial contractility; increased HR

 dosage: renal dose: 2-4ug/kg/min

inotropic effect: 5-10ug/kg/min

α-receptor effect: 10-20ug/kg/min

- 400mg Dopamine in 250ml D5W produces

1600ug/ml Dopamine

Verapamil (Ca+ channel blocker)

mech of action: blocks calcium access to the cells causing a decrease in contractility, decease
arteriolar constriction

dosage: 2.5 to 5mg IV over 2 min, repeat every 15-30min to a max of 20mg

Sodium bicarbonate

 to correct respiratory and metabolic acidosis

3. DEFIBRILLATION

Electrical counter shock

ASSESSMENT

Unresponsiveness,

cessation of respiration,

pallor, cyanosis,

absence of heart sounds/blood pressure/palpable pulse

Dilation pupils

Ventricular fibrillation or asystole (if on monitor)

NURSING INTERVENTION

Monitor arrest caused by ventricular fibrillation

 1. CPR until defibrillation is possible

 2. if defibrillation is unsuccessful, continue CPR and assist with administration of and

monitor effects of additional emergency drugs

 3. if defibrillation is successful, monitor client status

CARDIOPULMONARY RESUSCITATION (CPR)

Process of externally supporting the circulation and respiration of a person who has had a
cardiac arrest

NURSING INTERVENTION

1. Assess LOC

 Shake victim’s shoulder and shout

 If no response, summon help

2. Position victim supine on a firm surface

3. Open airway

 Use head tilt, chin lift maneuver

 Place ear over nose and mouth

Look to see is chest is moving

Listen for escape of air

Feel for movements of air against face

If no respiration, proceed with:

4. Ventilate twice, allowing for deflation between breaths

5. Assess circulation : palpate for carotid pulse; if not present proceed to:

6. initiate external cardiac compressions

Cardiac compression

A. proper placement of hands: lower half of the sternum

B. depth of compressions: 1 ½-2 inches for adults

C. 15 compressions (at rate of 80-100 per minute) with 2 ventilation

Acute Respiratory Failure

Sudden and life-threatening deterioration of the gas-exchange function of the lungs

Occurs when the lungs no longer meet the body’s metabolic needs

Acute Respiratory Failure

 Defined clinically as:

1. PaO2 of less than 50 mmHg

2. PaCO2 of greater than 5o mmHg

3. Arterial pH of less than 7.35

Acute Respiratory Failure

CAUSES

CNS depression- head trauma, sedatives

CVS diseases- MI, CHF, pulmonary emboli

Airway irritants- smoke, fumes

Endocrine and metabolic disorders- myxedema, metabolic alkalosis

Thoracic abnormalities- chest trauma, pneumothorax

Acute Respiratory Failure

PATHOPHYSIOLOGY

Decreased Respiratory Drive

Brain injury, sedatives, metabolic disorders à impair the normal response of the brain to normal
respiratory stimulation

Acute Respiratory Failure

PATHOPHYSIOLOGY

Dysfunction of the chest wall

Dystrophy, MS disorders, peripheral nerve disordersà disrupt the impulse transmission from the
nerve to the diaphragmà abnormal ventilation

Acute Respiratory Failure

PATHOPHYSIOLOGY

Dysfunction of the Lung Parenchyma

Pleural effusion, hemothorax, pneumothorax, obstructionà interfere ventilationà prevent lung

expansion

HEMOTHORAX
Acute Respiratory Failure

ASSESSMENT FINDINGS

Restlessness

dyspnea

Cyanosis

Altered respiration

Altered mentation

Tachycardia

Cardiac arrhythmias

Respiratory arrest

Acute Respiratory Failure

DIAGNOSTIC FINDINGS

Pulmonary function test- pH below 7.35

CXR- pulmonary infiltrates

ECG- arrhythmias

Acute Respiratory Failure

MEDICAL TREATMENT

Intubation

Mechanical ventilation

Antibiotics

Steroids

Bronchodilators

Acute Respiratory Failure

NURSING INTERVENTIONS

1. Maintain patent airway

 2. Administer O2 to maintain Pa02 at more than 50 mmHg

3. Suction airways as required

4. Monitor serum electrolyte levels

5. Administer care of patient on mechanical ventilation

CPAP

CEREBROVASCULAR ACCIDENTS
An umbrella term that refers to any functional abnormality of the CNS related to disrupted
blood supply

CEREBROVASCULAR ACCIDENTS

Can be divided into two major categories

1. Ischemic stroke- caused by thrombus and embolus

2. Hemorrhagic stroke- caused commonly by hypertensive bleeding

CEREBROVASCULAR ACCIDENTS

The stroke continuum

1. TIA- transient ischemic attack, temporary neurologic loss less than 24 hours duration

2. Reversible Neurologic deficits

3. Stroke in evolution

4. Completed stroke

General manifestations

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke

There is disruption of the cerebral blood flow due to obstruction by embolus or thrombus

RISKS FACTORS

Non-modifiable

Advanced age

Gender
 race

Modifiable

Hypertension

Cardio disease

Obesity

Smoking

Diabetes mellitus

hypercholesterolemia

Pathophysiology of ischemic stroke

Disruption of blood supply

Anaerobic metabolism ensues

Decreased ATP (adenosine triphosphate) production leads to impaired membrane function

Cellular injury and death can occur

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke

DIAGNOSTIC test

1. CT scan

2. MRI

3. Angiography

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke

CLINICAL MANIFESTATIONS

1. Numbness or weakness

2. confusion or change of LOC

3. motor and speech difficulties

4. Visual disturbance

5. Severe headache
 CEREBROVASCULAR ACCIDENTS: Ischemic Stroke

Motor Loss

Hemiplegia

Hemiparesis

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke

Communication loss

Dysarthria= difficulty in speaking

Aphasia= Loss of speech

Apraxia= inability to perform a previously learned action

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke

Perceptual disturbances

Hemianopsia

Sensory loss

paresthesia

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke

NURSING INTERVENTIONS

1. Improve Mobility and prevent joint deformities

Correctly position patient to prevent contractures

 Place pillow under axilla

 Hand is placed in slight supination- “C”

 Change position every 2 hours

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke

NURSING INTERVENTIONS

2. Enhance self-care

Carry out activities on the unaffected side

 Prevent unilateral neglect

Keep environment organized

Use large mirror

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke

NURSING INTERVENTIONS

3. Manage sensory-perceptual difficulties

Approach patient on the Unaffected side

Encourage to turn the head to the affected side to compensate for visual loss

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke

NURSING INTERVENTIONS

4. Manage dysphagia

Place food on the UNAFFECTED side

Provide smaller bolus of food

Manage tube feedings if prescribed

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke

NURSING INTERVENTIONS

5. Help patient attain bowel and bladder control

Intermittent catheterization is done in the acute stage

Offer bedpan on a regular schedule

High fiber diet and prescribed fluid intake

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke

NURSING INTERVENTIONS

6. Improve thought processes

Support patient and capitalize on the remaining strengths

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke

NURSING INTERVENTIONS

7. Improve communication

Anticipate the needs of the patient

Offer support

Provide time to complete the sentence

Provide a written copy of scheduled activities

Use of communication board

Give one instruction at a time

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke

NURSING INTERVENTIONS

8. Maintain skin integrity

Use of specialty bed

Regular turning and positioning

Keep skin dry and massage NON-reddened areas

Provide adequate nutrition

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke

NURSING INTERVENTIONS

9. Promote continuing care

Referral to other health care providers

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke

NURSING INTERVENTIONS

10. Improve family coping

11. Help patient cope with sexual dysfunction

CVA: Hemorrhagic Stroke

Normal brain metabolism is impaired by interruption of blood supply, compression and

increased ICP
 Usually due to rupture of intracranial aneurysm, AV malformation, Subarachnoid hemorrhage

CVA: Hemorrhagic Stroke

Sudden and severe headache

Same neurologic deficits as ischemic stroke

Loss of consciousness

Meningeal irritation

Visual disturbances

CVA: Hemorrhagic Stroke

DIAGNOSTIC TESTS

1. CT scan

2. MRI

3. Lumbar puncture (only if with no increased ICP)

CVA: Hemorrhagic Stroke

NURSING INTERVENTIONS

1. Optimize cerebral tissue perfusion

2. relieve Sensory deprivation and anxiety

3. Monitor and manage potential complications

CEREBRO-VASCULAR DISORDER:Stroke/Cerebrovascular Accident (CVA)

Definition: Disruption of the Blood Supply to the Brain-

-sudden loss of neurologic funtion

Note: Middle Cerebral Artery is commonly affected.

The second most frequently affected is the internal carotid artery.

Classification:

1. ischemic (a thrombus or embolus blocks circulation

2. hemorrhagic (a blood vessel ruptures)

Risk factors:

 Increased alcohol intake or cocaine

 Cardiac disease

 Cigarrette smoking

 DM

 Familial hyperlipidemia

 Family history of stroke

 Hx of TIA

 HPN

 Obesity,sedentary lifestyle

 Sickle cell disease

 Use of hormonal contraceptives

CEREBROVASCULAR ACCIDENTS

The stroke continuum

1. TIA- transient ischemic attack, temporary neurologic loss less than 24 hours duration

2. Reversible Neurologic deficits

3. Stroke in evolution

4. Completed stroke

Causes of Stroke:
Ischemic

 Thrombosis- occluded bld flow caused by thrombosis of the cerebral arteries supplying
the brain or the intracranial vessels

 The most frequent cause of CVA

 The most common cause of cerebral thrombosis is atherosclerosis; usually

affecting elderly persons.

 Tends to occur during sleep or soon after arising.

 This may tend to occur among clients with DM, and hypertension.
  Embolism- from thrombus outside the brain, such as in the heart, aorta, or common
carotid artery.

 The second most common cause of CVA.

 Most commonly affecting younger people.

 Most frequently caused by Rheumatic Heart Disease and MI.

 Symptoms occur at any time and progress rapidly.

 Causes of Stroke: Hemorrhagic Stroke

 Hemorrhage- Hemorrhagic Stroke

 Impaired cerebral perfusion from hemorrhage causes infarction, & the bld itself
as a space-occupying mass, exerting pressure on the brain tissues

 Hemorrhage from an intracranial artery or vein, such as HPN, ruptured

aneurysm, trauma, hemorrhagic disorder, or septic embolism.

 Transient Ischemic Attacks

 Refers to transient cerebral ischemia with

temporary episodes of neurologic dysfunction.

 Manifestation include contralateral weakness of the lower portion of the face,

fingers, hands, arms, and legs; dysphagia, and sensory impairment.

 Stoke in evolution refers to development of a neurologic deficit over several

hours to days

Pathophysiologic Changes in CVA:-specific manifestations are determined by the cerebral artery

affected, the brain tissue supply by that of that vessel, and the adequacy of the collateral
circulation

Aphasia, dysphasia; visual fields deficits; and hemiparesis of affected side (more severe in face
& arms)- resulting from thrombosis or hemorrhage of middle cerebral artery

Weakness, paralysis, numbness; sensory changes; altered LOC; bruits over carotid artery; and
headache caused by thrombosis or hemorrhage of carotid artery

Weakness, paralysis, numbness around lips & mouth; visual field deficits, diplopia, nystagmus;
poor coordination, dizziness, dysphagia, slurred speech; amnesia, and ataxia resulting from
thrombosis or hemorrhage of vertebrobasilar artery.
 Confusion, weakness, numbness; urinary incontenece; impaired motor & sensory functions; and
personality changes caused by thrombosis or hemorrhage of anterior cerebral artery.

Visual field deficits; sensory impairments; dyslexia; cortical blindness and coma resulting from
thrombosis or hemorrhage of posterior cerebral artery.

Assessment of CVA:
check for:

 S&S of increased ICP.

 Perceptual defects

 Aphasia

Unstable respiration

Severe headache

Diagnostic procedure results

Unilateral neglect

Diagnostic Findings:

CT scan- identifies an ischemic stroke within the first 72 hours of symptom onset or evidence of
a hemorrhagic stroke (lesions >1 cm immediately)

MRI-assists in identifying areas of ischemia or infarction and cerebral swelling

Others: angiography, carotid duplex scan,EEG

Complications:

Hemiplegia – weakness/paralysis of half the body

Cognitive impairement- Aphasia – maybe expressive or receptive; the partial or tota

inability to produce & understand speech

Apraxia – can move but cannot do the purpose; inability to perform complex
movements

Sensory impairement-Visual changes – homonymous hemianopsia; Agnosia – loss of sense of

smell

Dysarthria - difficulty in speech articulation due to lack of muscle control

Kinesthesia – loss of sensation (of bodily movement)

 Incontinence – maybe fecal/urine; inability to control urination or defecation

Shoulder pain

Contractures

Fluid imbalances

Cerebral edema

Aspiration

Altered LOC

Infections such as pneumonia

Nursing Considerations:CVA

 Maintain a patent airway and oxygenation:

If the pt is unconscious; vomiting- lateral position to prevent aspiration of saliva

 Check v/s & neurologic status:

Monitor BP, LOC, pupillary changes, motor and sensory functions, speech, skin, color, temp.

Monitor pt for s/s of increased ICP and nuchal rigidity or flaccidity

 Watch for s/s of pulmonary emboli:

chest pain, shortness of breath, dusky color, tachycardia, fever, and change in sensorium

 If the pt is unresponsive, monitor ABG as ordered

 Monitor F & E balance:

Monitor I and O.

Administer IVF as ordered

Offer bedpan /urinal

 .

Nursing Considerations:CVA

 Ensure adequate nutrition:

Check for gag reflex before offering small oral feedings of semisolod food
Teach the client to chew on the unaffected side.

If oral feeding is not possible,TPN, NGT feeding, gastrostomy feeding.

 Turn the patient frequently, at least q 2 hrs to prevent pneumonia.

 Perform ROM exercises for affected & unaffected sides.

 Massage if not contraindicated.

 Provide meticulous eye care- Instill meds as ordered; patch the affected eye if the pt can’t close
eyelid.

Nursing Considerations:CVA

 Compensate for perceptual difficulties.

 Care of the client with Hemianopsia.

 Approach from the unaffected side.

 Place articles on the unaffected side.

 Promote communication

 Care for the client with aphasia.

 Say one word at time.

 Give simple commands.

 Allow the client to verbalize, no matter how long it takes him

Give medications as ordered- Tell the pt to watch out for side effects. (ex. Aspirin-GI bleeding

Assist with rehab

Teach the pt to comb hair, to dress, & to wash

Obtain assistive devices ( through the aid of PT/OT) such as walkers, hand bars by the toilet, and
ramps as needed

Be aware that the pt has a unilateral neglect, in which he fails to recognize that he ha a paralized
side- show him how to protect his body from harm

Emphasize importance of regular ff-up visits

 Diabetic Ketoacidosis
This is cause by the absence of insulin leading to fat breakdown and production of ketone
bodies

Three main clinical features:

 1. HYPERGLYCEMIA

 2. DEHYDRATION & electrolyte loss

 3. ACIDOSIS

DKA

PATHOPHYSIOLOGY

No insulinà reduced glucose breakdown and increased liver glucose production à

Hyperglycemia

DKA

PATHOPHYSIOLOGY

Hyperglycemiaà kidney attempts to excrete glucose à increased osmotic load à diuresis à

Dehydration

DKA

PATHOPHYSIOLOGY

No glucose in the cellà fat is broken down for energy à ketone bodies are producedà
Ketoacidosis

DKA

Risk factors

1. infection or illness- common

2. stress

3. undiagnosed DM

4. inadequate insulin, missed dose of insulin

DKA

ASSESSMENT FINDINGS
 1. 3 P’s

2. Headache, blurred vision and weakness

3. Orthostatic hypotension

DKA

ASSESSMENT FINDINGS

4. Nausea, vomiting and abdominal pain

5. Acetone (fruity) breath

6. Hyperventilation or KUSSMAUL’s breathing

HYPERGLYCEMIA

Hyperglycemia

DKA

LABORATORY FINDINGS

1. Blood glucose level of 300-800 mg/dL

2. Urinary ketones

DKA

LABORATORY FINDINGS

3. ABG result of metabolic acidosis- LOW pH, LOW pCO2 as a compensation, LOW bicarbonate

4. Electrolyte imbalances- potassium levels may be HIGH due to acidosis and dehydration

DKA

NURSING INTERVENTIONS

1. Assist in the correction of dehydration

 Up to 6 liters of fluid may be ordered for infusion, initially NSS then D5W

 Monitor hydration status

 Monitor I and O

 Monitor for volume overload

 DKA

NURSING INTERVENTIONS

2. Assist in restoring Electrolytes

 Kidney function is FIRST determined before giving potassium supplements!

DKA

NURSING INTERVENTIONS

3. Reverse the Acidosis

 REGULAR insulin injection is ordered IV bolus 5-10 units

 The insulin is followed by drip infusion in units per hour

 BICARBONATE is not used!

HHNS
A serious condition in which hyperosmolarity and extreme hyperglycemia predominate

Ketosis is minimal

Onset is slow and takes hours to days to develop

HHNS

PATHOPHYSIOLOGY

Lack of insulin action or Insulin resistance à hyperglycemia

Hyperglycemiaà osmotic diuresis à loss of water and electrolytes

HHNS

PATHOPHYSIOLOGY

Insulin is too low to prevent hyperglycemia but enough to prevent fat breakdown

Occurs most commonly in type 2 DM, ages 50-70

DIFFUSION AND OSMOSIS

HHNS
Precipitating factors

1. Infection

2. Stress

3. Surgery

4. Medication like thiazides

5. Treatment like dialysis

HHNS

ASSESSMENT FINDINGS

1. Profound dehydration

2. Hypotension

3. Tachycardia

4. Altered sensorium

5. Seizures and hemiparesis

HHNS

DIAGNOSTIC TESTS

1. Blood glucose- 600 to 1,200 mg/dL

2. Blood osmolality- 350 mOsm/L

3. Electrolyte abnormalities

HHNS

NURSING INTERVENTIONS

Approach is similar to the DKA

1. Correction of Dehydration by IVF

2. Correction of electrolyte imbalance by replacement therapy

HHNS

NURSING INTERVENTIONS
3. Administration of insulin injection and drips

4. Continuous monitoring of urine output