Transcript Lower Respiratory Disorders

Lower Respiratory Disorders
Continued
Pulmonary edema - Aspiration
Pulmonary edema
• Rapid shift of fluid from
the plasma to pulmonary
interstitial tissue and
alveoli
• Causes impaired gas
exchange
Pulmonary edema
• d/t
– left ventricular failure 
– Backed up blood in the
pulmonary vein 
– h pressure in pulmonary
vascular system 
– Fluids “leak” into interstitial
space & alveoli
Pulmonary edema
Etiology / Contributing
factors
• Left ventricular failure
• Fluid overload
– IV’s
• Drug OD
Pulmonary edema
Clinical Manifestations
• Dyspnea
– Sudden
– Orthopnea
– Cyanotic (central)
– “air hunger”
– Tachypnea
• Cough
– Copious sputum
– Frothy
– Blood tinged
Pulmonary edema
Clinical Manifestations
• Pulse
– Tachycardia
– Bounding
• BS
– Crackles
• Fine  course
• Engorged neck & hand
veins
Pulmonary edema
Clinical Manifestations
• Anxiety
• Confusion
• Stupor
Pulmonary edema
Diagnostic exam
• Auscultation
– Crackles
• X-ray
• V/S
– Tachycardia
– Tachypnea
• Pulse oximetry
– i
• ABG’s
– PaO2
• i
Pulmonary edema
Treatment
• Goal:
– Remove fluid
– h oxygenation
• O2
– Mask
• Non-rebreather
• Mech. Vent
– PEEP
Pulmonary edema
• Diuretics
– Lasix
• Digitalis / Digoxin lanoxin
Bronchodilators
– Aminophylline
• Morphine
– i peripheral resistance 
– i pressure in pulmonary
capillaries 
– i leakage
– i anxiety
Pulmonary edema
•
A.
B.
C.
D.
E.
Which of the following electrolytes must be
closely monitored in a patient on Lasix
diuretic therapy?
Chloride
Hydrogen
Magnesium
Potassium
Sodium
Pulmonary edema
• What nursing actions must be performed
before administering digitalis?
– This is not multiple choice – you should know this
one cold!
• What do you do if the apical pulse is <60?
Pulmonary edema
Diagnosis:
• Impaired Gas Exchange: the fluid –filled alveoli decreases
the exchange of gases
Out come:
• the client will demonstrate improved gas exchange, as
evidenced by rising PO2 to 55 or 60 mm Hg, Oxygen
saturation above 90%, normaralizing pH, decreasing anxiety
and dyspnea, and fewer crackles
Pulmonary edema
Nursing management
• Diet
– Sodium
• Low
– Potassium
• High
– Fluids
• Decreased / restricted
• I&O
• Weights
– Q day
Pulmonary edema
Nursing management
• Position to promote
circulation
– HOB h
– Dangle legs
Pulmonary edema
Nursing management
• Provide psychological
support
• Monitor meds
Acute Respiratory Failure
Definition
• Sudden & life-threatening
• i gas exchange
“It exists when the exchange of O2
for CO2 in the lungs cannot keep
us with the rate of O2
consumption & CO2 production.”
• Ventilation & Perfusion are
impaired
Acute Respiratory Failure
ABG’s
• PaO2
– < 50 mmHg
• PaCO2
– > 50 mmHg
• Arterial pH
– < 7.35
Acute Respiratory Failure
Causes of ARF
• i respiratory drive
– TBI, MS, Sedatives,
hypothyroidism
• Dysfunction of the chest
wall
– Nerve, spinal cord,
neuromuscular junction
disorders
• Dysfunctional Lung
Parenchyma
Acute Respiratory Failure
S&S
• Early
–
–
–
–
–
Restlessness
Fatigue
H/A
Dyspnea
Respirations
• Air hunger
– Pulse
• h
– BP
• h
Acute Respiratory Failure
S&S
• Progresses
–
–
–
–
Confusion
Central cyanosis
Diaphoresis
Resp. arrest
Acute Respiratory Failure
Nursing management
• Assist with intubation &
maintain mechanical
ventilation
• Assess respiratory status
–
–
–
–
LOC
ABG’s
SpO2
VS
Acute Respiratory Failure
Nursing management
• Implement strategies to
prevent complications
–
–
–
–
TCDB
Oral care
Skin care
ROM
• Address problems that led
to ARF
Acute Respiratory Distress Syndrome
• AKA
– ARDS
– Adult Respiratory
distress syndrome
Acute Respiratory Distress Syndrome
•
•
•
•
ARDS is acute,
Severe injury to most or all of both lungs.
ARDS is not a specific disease;
ARDS can be confused with congestive heart
failure
• IT is respiratory failure that occurs as a result
of massive trauma to the lungs
Acute Respiratory Distress Syndrome
•
Characterized by
–
–
–
–
–
•
•
sudden and progressive pulmonary edema
increasing bilateral infiltrates on chest x-ray
Hypoxemia
reduced lung compliance
Not due to left side heart failure
Occurs as a result of injury to alveolar
capillary membrane
(D/T: aspiration, drug OD, smoke, infection,
shock, trauma, sepsis*)
Acute Respiratory Distress Syndrome
•
•
•
•
•
Injury 
Inflammatory response 
release chemical (histamine etc.) which
cause injury to the alveolar capillary
membrane 
Leakage of fluid into the alveolar interstitial
space and alt. Capillary beds
Protein, blood cells and fluid enter alveoli 
Acute Respiratory Distress Syndrome
• Decrease in surfactant 
• Alveoli collapse (atelectasis) and fibrotic changes

• Lungs become stiff, less compliant, very hard to
inspire 
• Decrease in gas exchange /shunted 
• Hypoxia 
• Atelectasis and edema worsen 
• Lungs may hemorrhage
Acute Respiratory Distress Syndrome
•
Etiology/Contributing factors
–
–
–
–
–
Infection
Trauma
Narcotic OD,
Inhalation of irritants
Aspiration
Acute Respiratory Distress Syndrome
•
Clinical manifestations
–
Rapid onset of severe dyspnea
•
•
•
•
–
with in 12-48 hours
Intercostal and suprasternal retractions
Increased resp rate
Crackles
Hypoxemia that does not respond to O2
•
•
•
Confusion anxiety
Restlessness, apprehension
Cyanosis
Acute Respiratory Distress Syndrome
– ABG’s
• PaO2
– < 70mmHg
• PaCO2
– > 35
• HCO3
– Normal
– < 22
• pH
– low
• Analysis
– Resp. and met. Acidosis
Acute Respiratory Distress Syndrome
•
Diagnostic exams/procedures
–
X-ray
•
appears to be white due to excessive fluid in the
lungs
Acute Respiratory Distress Syndrome
•
Treatment
–
O2 Intubation and mechanical vent.
•
–
Maintain PaO2 at > 60mm Hg
PEEP
•
•
•
•
–
Improves oxygenation
Increases functional residual capacity
Reverse alveolar collapse
Use a lower FiO2
Systemic hypotension
•
Fluid leakage
Acute Respiratory Distress Syndrome
–
–
–
–
Pulmonary vasodilators
Surfactant replacement
Corticosteroids
Sedatives
• due to anxiety and ventilator
– Diuretics
– Circulatory support
• Adequate fluid volume
– May limit fluids
– Nutritional
– Neuromuscular blockers / paralytic drugs
Acute Respiratory Distress Syndrome
•
Nursing intervention
–
–
Rest
Change position
•
monitor O2 sat in different positions
–
–
•
High fowlers
Prone
Complications
–
–
High death rate (50-60%)
No one recovers 100%
Pulmonary Hypertension
•
Pathophysiology
–
Pulmonary arteries narrow
•
–
Vasoconstriction
Increased Pulmonary BP
•
–
(>30 mmHg)
How do you measure pulmonary BP?
•
Only can be measured during right side heart
catheterization
Pulmonary Hypertension
• Pathophysiology
– If increase in BP 
– Right ventricle has to work harder
– Right ventricle hypertrophy
• enlargement and dilation 
– Right ventricle fails
• Precursor to Cor Pulmonale
Pulmonary Hypertension
•
Etiology/Contributing factors
–
Primary:
•
•
•
•
•
–
Rare
Female > Male
Age 20-40 years
hereditary tendency
usually die within 5 years of diagnosis
Secondary:
•
Existing cardiac or pulmonary disease
–
–
Mitral valve disease
COPD
Pulmonary Hypertension
•
Clinical manifestations of
–
Pulmonary hypertension without right sided
heart failure
•
•
•
•
(Not clinically evident until late in progression)
Dyspnea and fatigue that worsens over time
Cyanosis and Tachypnea
Crackles and decrease breath sounds
Pulmonary Hypertension
• Clinical manifestations of…
– Right sided heart failure
•
•
•
•
•
•
Peripheral edema
Ascites
Distended neck veins
Liver engorgement
Crackles
Heart murmur
Pulmonary Hypertension
•
Diagnostic exams/procedures
–
ABG’s:
•
PaO2
–
–
•
Decreased
Hypoxemia
PaCO2
–
–
Increased
Hypercapnia
Pulmonary Hypertension
• Diagnostic exams
– ECG
• Shows right ventricular hypertrophy
– Cardiac catheterization
• Right sided heart catheterization only way to measure
pulmonary pressure
– X-ray
– Pulmonary function test
Pulmonary Hypertension
•
Treatment
–
–
–
Oxygen therapy
Vasodilators (in some people)
Anticoagulants –
•
–
–
Warfarin (Coumadin)
Diuretic to decrease blood volume
Heart/lung transplant
–
Really there is no cure – death within 2-3 years of diagnosis
unless transplant
Pulmonary Hypertension
• A 66-year-old client takes a potassiumdepleting diuretic. Foods that will help to
keep the client’s potassium level within
normal limits include
–
–
–
–
–
–
Bananas
Oranges
Cantaloupe
fish
Spinach
whole-grain cereals
Pulmonary Heart Disease
• Pathophysiology
– Right ventricular failure d/t increased
pulmonary pressure
– Pulmonary artery vasoconstriction
– Right ventricle has to work harder
– Right ventricle fails
Pulmonary Heart Disease
– Right ventricle does not empty normally
– Backward buildup
– Increase in Right atrial and systemic venous blood
volume
– Jugular neck veins distend
– Peripheral edema
– Angina from right ventricle ischemia
Pulmonary Heart Disease
• Clinical Manifestations (right vent. failure)
– Edema
• Feet
• Legs
– Distended neck veins
– Enlarged palpable liver
– Pleural effusion
– Ascites
– Heart murmur
Pulmonary Heart Disease
• Medical treatment
– Improve ventilation
• Treat lung disease
• Treat heart disease
– Lung disease
• O2
• Chest physiotherapy
• Bronchial hygiene
• Intubation
– Heart disease
• Bed rest
• Na restriction
• Diuretic
• Digitalis
Pulmonary Heart Disease
• Nursing management
– Monitor ventilators
– Monitor heart and lungs
•
•
•
•
O2
Na Restriction diet
Diuretics
Stop smoking
Pulmonary Emboli
Pathophysiology
•
Emboli:
–
foreign object that
travels through the
blood stream
•
•
•
•
blood clot
Air
Fat
Thrombus (thrombi – pl)
–
A stationary clot
Pulmonary Emboli
• Emboli travels into a pulmonary
artery causing obstruction
– Ventilation/perfusion mismatch
• Ventilation
– Yes
• Perfusion
– no
– CO2
• h
• respiratory acidosis
Pulmonary Emboli
Etiology/Contributing factors
•
Most PE originate in
deep veins of the lower
extremities
•
Deep Vein Thrombosis
– DVT
Pulmonary Emboli
S&S of DVT
•
Positive Homan’s sign
–
Pain w/ passive
dorsiflexion
•
calf tenderness & swelling
•
Unilateral
•
Warm distal extremities
•
Skin discoloration
•
Superficial vein distention
Pulmonary Emboli
•
A.
B.
C.
Does a person with DVT have pedal pulses?
Yes
No
I think I’ll just wait for Mrs. Keele to reveal
the answer!
Pulmonary Emboli
Risk Factors for DVT
•
Surgery w/ general
anesthesia
•
Fx of the lower extremities
•
Heart failure
•
Bed rest / paralyses
•
Obesity
•
Amniotic Fluid Embolism
and air embolism
Pulmonary Emboli
Prevention of DVT
•
Leg exercises
•
X sitting cross legged
•
Drink fluids
•
Anticoagulant therapy
Pulmonary Emboli
Complications of Anticoagulant
therapy
•
Wear shoes
•
Use an electric razor
•
Use a soft toothbrush
•
Easy bruising
•
Nose bleeds
•
Bleeding that does not stop
Pulmonary Emboli
• Blood in urine
• Blood in sputum
– black stools
• Changes in menstrual flow
• Avoid aspirin
• Lab work on time
• If lactating an infant
– P baby for S&S too
• Elderly
– Close monitoring
Pulmonary Emboli
Treatment of DVT
•
naturally dissolves
–
7-10 days
•
Bed rest
–
strict!
•
Anticoagulant therapy
–
Heparin
•
Route?
–
–
–
–
IV
Sub q
never IM
Warfarin Sodium/
Coumadin
Labs?
–
•
PTT/PT
Pulmonary Emboli
• O2
• Thrombolytic agents
– Streptokinase
– Urokinase
Pulmonary Emboli
Clinical manifestations of PE
•
Sudden onset
–
Dyspnea
–
Tachypnea
–
sharp chest pain
–
Cough
–
Hemoptysis
•
Gasping for breath & anxious
•
Death with in one hour!
•
Venous return is
–
i
–
Jugular venous distention
Pulmonary Emboli
• ABG’s:
– PaO2
• i
– PaCO2
• h
• Hypocapnia
– pH
• i
• Respiratory Acidosis
Pulmonary Emboli
Dx exams/procedures
•
Lung scan
•
Pulmonary angiogram
•
ABG’s
•
CT*
•
MRI*
–
* only show if large
Pulmonary Emboli
Nursing intervention
•
Assess resp distress / function
•
ID patients at risk
–
ambulation
–
range of motion
–
sequential/ted hose
•
Assess for Homan’s sign
•
P heart failure
•
Educate about
–
anticoagulant therapy
–
Prevention
–
S&S
Pulmonary Emboli
•
•
•
•
•
•
•
•
•
•
Avoid leaving IV catheters in for
long time
If SOB, HOB h
O2 as prescribed
Pulse Oximetry
Opioids for sever pain
Anticoagulation per MD
– Monitor for complications
Enc. to verbalize fear
Nebulizer tx
I.S.
Chest physiotherapy
Pulmonary Emboli
Complications
•
Right ventricle unable to
push blood into the
occluded artery 
•
Weak contractions 
•
i cardiac output 
•
Hypotension
•
Increase BP within the
pulmonary circulation 
•
Right ventricular failure 
•
Cor Pulmonale
Sarcoidosis
• Pathophysiology
– A granulomatous disease that affects many body
systems
– A tumor like mass or nodule of granulation tissue
•
due to chronic inflammatory process
– Hypersensitivity response to one or more agents
Sarcoidosis
• Clinical manifestations
–
–
–
–
–
–
–
–
Insidious onset – lack of prominent S&S
Dyspnea
Cough
Hemoptysis
Congestion
Anorexia
Fatigue
Weight loss
Sarcoidosis
• Assessment & Dx
– X-ray
– CT scan
– Biopsy
– ABG’s
• Varied
– Normal
– Hypoxemia
– Hypercapnia
Sarcoidosis
• Medical management
– Remission without specific treatment
– Corticosteroids
Pneumoconioses
•
•
•
•
•
–
–
–
–
–
–
–
–
Occupational lung disease
Pathophysiology
Non neoplastic alteration of the lung
secondary to exposure to inorganic dust
Silicosis
silica dust
mining, quarrying and tunneling operators
Asbestosis
Asbestos
Dust
no cure
Coal workers pneumoconiosis
Black Lung disease
Lung Cancer
Pathophysiology
•
Carcinogen binds to
the DNA and changes
it
•
Abnormal growth
•
Usually develops on
the wall of the
bronchial tree
FYI
• Lung Cancer is the number one cancer killer in
the US
Lung Cancer
Etiology/Contributing factors
•
#1
–
Tobacco Smoke (85%)
–
Second hand smoke
•
Carcinogens
–
Asbestos
–
Uranium
–
Arsenic
–
Nickel
–
Iron oxide
–
Radon
–
Coal dust
Lung Cancer
Clinical manifestations: early
•
Insidiously and
asymptomatic until late
stages
FYI
– 70% of lung CA have metastasized by the time of
diagnosis
Lung Cancer
S&S: Early
• Objective symptoms
– #1:
• Cough
– #2
• Repeated respiratory
tract infection
– Wheezing
– Dyspnea
Lung Cancer
S&S: Late
•
Hemoptysis
•
Chest pain
•
Pleural friction rub
•
Pleural effusion
•
Finger Clubbing
•
Wt loss
•
Anemia
•
Anorexia
Lung Cancer
•
A.
B.
C.
D.
E.
F.
When Lung cells mutate due to cancer, they frequently
produce and secrete what endocrine hormone?
ACTH
T3 (thyroxin)
FSH
ADH
Insulin
Growth hormone
Lung Cancer
• An increase secretion of ADH due to lung
cancer is diagnosed as what disorder?
– No hints this time, can you name it?
– Turn to your neighbor and show them how smart
you are!
Lung Cancer
Dx exams/procedures
•
X-ray
•
CT scan
•
Biopsy via
Bronchoscopy
Lung Cancer
Treatment
•
Removal of Ca tumor
•
Chemotherapy
–
•
Metastasis
Radiation
–
To shrink or reduce
symptoms
Lung Cancer
• Nursing intervention
–
–
–
–
–
–
Dyspnea
Anorexia
Pain control
Fatigue
Grief
Hospice
• Preventative measures
– #1
•
Stop smoking
Lung Cancer
Clients receiving chemotherapy
• Enc client to eat soft, non-irritating foods high in protein
• Watch for S/E of chemotherapy and radiation
• Administer antiemetics and anti-diarrheals
• Provide good skin care
• Reverse isolation
– Leukopenia
– neutrophil
• Stomatitis
– inflammation of the mucous membranes of the mouth
Lung Cancer
•
A.
B.
C.
D.
E.
A client with cancer of the lung is receiving chemotherapy. The nurse
will monitor blood values especially:
RBC
WBC
PT/PTT
K+ & ClThese drugs depress the bone marrow, inhibiting the production of
blood cells, and a serious decrease in WBC’s increases susceptibility to
infection
Chemotherapy Question?
The most likely side effect of chemotherapy is:
A. Fatigue
B. Nausea
C. Dehydration
D. Skin ulceration
Question?
A 40-year-old man has developed Stomatitis after chemotherapy
treatment. He should be encouraged to:
A. Eat hot, spicy foods
B. Brush his teeth after each meal and at bedtime
C. Rinse his mouth with commercial mouthwash after each
meal
D. Drink plenty of orange juice
Question?
A 62-year-old client is receiving radiation treatments for lung cancer. The
field for radiation therapy is clearly outlined with purple ink. The nurse
would treat this field as follows:
a.
Bathe it the same as any other part of the body
b.
Apply moisturizing lotion to prevent dryness
c.
Wipe is with clear water and pat dry as needed only
d.
Treat as a stage 1 decubitus ulcer
Question?
Cancer pain is best managed with the use of
A. A patient-controlled analgesia pump
B. Short-acting opioids administered around the clock
C. Frequent administration of breakthrough medications
D. Long-acting opioids administered around the clock
Question?
A client taking opiods for cancer pain begins to
require more medication to provide the
same amount of analgesia. This is known as
A. Physical dependence
B. Drug tolerance
C. Addiction
D. Equianalgesia
Lung Cancer
Preventative measures
•
Stop smoking
Lung Cancer
•
Complications
–
–
–
–
–
Pleural effusion
Tumor obstructs Superior vena Cava
Ectopic hormone Production
• mimics the bodies own hormones
• ADH (anti diuretic hormone) = SIADH (syndrome of
inappropriate ADH) No urine output
• ACTH (Adrenocorticotropic hormone) = Cushing syndrome
Atelectasis & Pneumonia
Metastasis (brain, bone, lung, liver, lymphnodes)
Rib fractures
• Pathophysiology
– usually 4th – 9th rib
– If 1-3 rib high mortality rate
• Etiology/Contributing factors
–
–
–
–
Blunt vs. Penetrating
Spleen and liver damage
Trauma
Uncontrolled coughing
Rib fractures
• Clinical manifestations
– Pain
•
•
Severe
aggravated by
– Movement
– Breathing
– coughing
–
–
–
–
Ecchymosis
Crepitus
Swelling
Deformity
Rib fractures
• Diagnostic exams/procedures
–
–
–
–
X-ray
ECG
O2 SATs
ABG’s
Rib fractures
• Treatment
– Detect and treat other injuries
– Do Not use elastic rib belts
•
(decrease breathing)
– Control pain
•
•
•
so TCDB
decrease complications
If needed an intercostal nerve block
– Ribs generally heal in about 6 weeks
– Ice packs
Flail chest
• Pathophysiology
– When multiple ribs are fractures, structural
support of the chest is impaired
– Ribs are fractures at 2 or more sites
Flail chest
– Paradoxical respiration
• Normal – I
– Chest expands
• Normal – E
– Chest shrinks
• Flail chest – I
– Area of flail chest collapses
• Flail chest – E
– Area of flail Chest bulges
– Ineffective ventilation
• Hypoxia
Flail chest
•
S&S
–
–
–
–
–
Dyspnea
Anxious
Tachypnea
Tachycardia
Paradoxical respiration
•
Expiration:
–
–
•
Flail bulges
mediastium
» affected side
Inspiration:
–
–
Flail collapses
mediastium
» unaffected side
Flail chest
• Treatment
– Decrease the work load of breathing
•
•
•
Oxygen
Intubation
Mech. Ventilation
– Chest tubes?
– Stabilize chest
•
severe