ACUTE RESPIRATORY FAILURE.pdf

Running head: ACUTE RESPIRATORY FAILURE

Acute Respiratory Failure

Jack Green

Liberty University

ACUTE RESPIRATORY FAILURE

Patient Profile Worksheet

A. Personal Information

Room # 572 Gender: F Ethnicity: white Age if < 90: 81

Place of Residence: Forest MD: Dr. Guillermo

EmergencyContact Spouse MaritalStatus: Married

Admitting Diagnosis: Acute Respiratory Failure

Co-Morbidities: Hypertension, Hyperlipidemia

Date of Admission: 3/31/17 Date of Surgery: N/A Allergies: Sulfa

Code Status: DNR Mental Status: oriented x4

B. Activity and Nutrition

Diet order: Cardiac Route/Rate: mealtime Last Wt: 66 kg

Level of Activity (bedrest, up ad lib, BRP, turning): bedrest

Level of self-care: Assist x1

C. Nursing Care:

Drainage devices (foley, NGT, JPs, T-tube, etc): N/A

NGT Flushes: N/A

Wound care/Dressing (be specific): pressure on buttocks (foam pad), skin tear arm

(guaze), lower leg skin tear (guaze)/

IV access (peripheral, central, location, care): left upperarm 20 guage

IVF: @ mL/hr Saline Lock: Yes TPN: N/A

Frequency of vital signs (including pulse oximetry): Q4H

Frequency of Glucometer: N/A Supplemental oxygen: 25 L heated nasal canula OSA: not

identified

Falls Risk: High risk

Precautions: The patient is a high falls risk.

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Most Recent Labs (include date of labs):

Common Hematology/Chemistries/RFTs

Date of Labs Taken 3/18 3/21

Na 137 136-145 mEq/L

K 4.3 3.5-5.1 mEq/L

Cl 99 98-110 mEq/L

TCO223 20-28 mEq/L

Anion Gap 15 5-15 mEq/L

Glucose 118 H 70-100 mg/dL

Urea Nitrogen 30 H 5-23 mg/dL

Creatinine 1.5 H 0.5-1.3 mg/dL

Ca+2 9.9 8.5-10.4 mg/dL

GFR 33L >60mL/min/1.73m

RBC 5.12 4.20-5.50 m/uL

Hgb 16.0 14.0-18.0 g/dL

HCT 49.1 41.0-51.0%

WBC 11.9 H 4.0-10.0 k/uL

Platelet 279 150-450 k/uL

Other Pertinent Labs (make sure to document important trends):

Blood pH: 7.27 PaCO2: 51.8 mm Hg HCO3- : 20.5 mEq/L

Patient History Worksheet:

Chief Complaint: Chest Pain

History of Present Illness (discuss clinical course from admission until current date):

Patient 572 is an 81 year old female with a history of breast cancer and two bilateral

mastectomies. She came to the ER reporting a loss of appetite and sweats for 3 days. She also

reported an onset of chest pain the day before she came to the hospital. She said it was on the left

side of her ribs and back. The pain has progressively getting worse. A small mass was also found

on the anterior mediastinum. Upon her admission oxygen stats and blood pressure were also low.

ACUTE RESPIRATORY FAILURE

Her arterial blood gases also showed evidence of metabolic acidosis possibly due to her acute

kidney injury. It was suspected that she had pneumonia show her blood cultures were taken and

she was put on broad spectrum antibiotics until the results returned. The results of the blood

cultures showed evidence of Haemophilus influenzae bactremia and it was determined that she

had left lower quadrant, community acquired pneumonia. She was then prescribed a 6 day course

of Ceftriaxone. The patient also began to show evidence of of metabolic encephalopathy due to

acute infection causing AKI. The patient was hypoxemic and hypercarbic. She showed sigs of

acute hypoxemic respiratory failure.

Past Medical History:

The patient’s medical history includes breast cancer, Esophageal dilations, possible CVA

Past Surgical History:

The patient’s past surgical history includes Dilation of esophagus, bilateral mastectomy

Family History:

No significant family history

Tobacco: none Alcohol: none Illegal Drugs: none

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Occupational Status: none

Religious Preference: none

Cultural Support Needs: none

ACUTE RESPIRATORY FAILURE

Acute Respiratory Failure

Patient 572 is an 81-year-old female with a history of breast cancer and two bilateral

mastectomies. She came to the ER reporting a loss of appetite and sweats for 3 days. She also

reported an onset of lower chest pain the day before she came to the hospital. She said it was on

the left side of her ribs and back as well. The pain has been progressively getting worse so she

presented to the emergency department for evaluation. A small mass was also found on the

anterior mediastinum. Upon her admission, oxygen stats and blood pressure were also low. Her

arterial blood gasses also showed evidence of metabolic acidosis possibly due to her acute

kidney injury. Her creatinine level was 1.5 mg/dL and her blood urea nitrogen (BUN) was 30

mg/dL. Her white blood cell count was also 11.9 k/uL, which is slightly elevated. It was

suspected that she had pneumonia show her blood cultures were taken and she was put on broad

spectrum antibiotics until the results returned. The results of the blood cultures showed evidence

of Haemophilus influenzae bactremia and it was determined that she had left lower quadrant,

community-acquired pneumonia. She was then prescribed a 6-day course of Ceftriaxone. The

patient also began to show evidence of metabolic encephalopathy due to acute infection causing

AKI. The patient was hypoxemic and hypercarbic. She showed signs of acute hypoxemic

respiratory failure.

Pneumonia describes the inflammatory process of the parenchymal structures of the

lower respiratory tract. Pneumonia is the sixth leading cause of death in the United States and is

the most common cause of death due to an infectious disease. Because of the overlap of

symptomology and variation in the spectrum of infectious organisms involved, pneumonia is

generally classified by the setting in which it develops. This is characterized as either

community or hospital acquired pneumonia. People with a compromised immune system make

ACUTE RESPIRATORY FAILURE

them vulnerable to developing pneumonia in both of these categories. Pneumonia can also be

classified by the agent causing the infection. Which can be atypical or typical. Typical

pneumonias are the result from infection by bacteria that multiply rapidly in the alveoli, causing

inflammation in the lower respiratory tract and exudation of fluid into the air-filled spaces.

Atypical pneumonia is caused by viral and mycoplasma infections that involve the alveolar

septum and the interstitium of the lungs. This type of Pneumonia usually does not produce the

obvious symptoms of typical pneumonia such as a high WBC count, purulent sputum, and

consolidation. It is also a lot harder to detect with a chest x-ray. The last classification of

pneumonia is based on where the infection is distributed in the lungs. This classification is only a

classification for typical pneumonias. Typical pneumonia is classified as lobar pneumonia or

bronchopneumonia. Lobar pneumonia describes consolidation in part of a single lung lobe or all

of a lung lobe. Bronchopneumonia is a spread out consolidation of more than one lobe. Since the

patient had consolidation in her lung bases, This created a reduced surface area for the exchange

of oxygen and carbon dioxide. Because CO2 is acidic in nature, this contributed to the patient’s

acidosis since the CO2 was not able to leave the blood stream due to fluid-filled alveoli. The

consolidation also caused the patient’s shortness of breath and a low oxygen saturation of 91%

on admission. To help the patient remove the sputum from the lower lung fields, she was

encouraged to cough and deep breathe to propel the fluid out of her lungs (Grossman, 2014,

Disorders of Ventilation and Gas Exchange).

The patient was diagnosed with typical community-acquired pneumonia. Community-

acquired is used to describe infections found in the outside of the hospital rather than in the

hospital. It is defined as pneumonia that is diagnosed within 48 hours of admission to the

hospital in a person who has not been a resident of long term care facility for more than 14 days

ACUTE RESPIRATORY FAILURE

before admission. The lungs below the main bronchi is usually a sterile environment despite the

frequent entry of microorganisms because of aspiration of nasopharyngeal secretions. The

aspiration of microorganisms can colonize in the upper airway when relaxing or during sleep.

Usually, these organisms do not cause significant problems because there is only a small amount

so the respiratory tract’s defense mechanisms such as the mucous escalator and the nares.

Damage to the ciliary endothelium that lines the respiratory tract and impaired immune response

can predispose the lungs to the colonization of bacteria and infection in the lower respiratory

tract. (Grossman, 2014, Disorders of Ventilation and Gas Exchange).

The bacteria that caused the pneumonia in the patient’s left lung was Haemophilus

influenzae bacteremia. The transmission of H influenzae is either by direct contact or by

inhalation of respiratory tract droplets. This was evidenced by a slightly raised white blood cell

count of 11.9 k/uL. The normal range is between 4.0 and 10.0 k/uL A larger bacterial load or the

presence of a viral infection can potentiate this infection. Since the influenza has been prevalent

in the recent months, it is very possible that the patient had a viral infection that led to the

colonizing of bacteria invaded the respiratory mucosa and entered the bloodstream. The presence

of antibodies and phagocytes determines how well the bacteremia is cleared from the lung fields.

The antiphagocytic nature of the Haemophilus influenzae capsule and the absence of the anti-

capsular antibodies lead to increasing bacterial proliferation. When the bacterial concentration

rises to a critical level, it can disseminate to various sites, including pleura, pericardia, and lungs

(Devarajan, 2016).

The driving force for glomerular filtration is the pressure gradient from the glomerulus to

the Bowman space surrounding the glomerulus. Glomerular pressure depends primarily on renal

blood flow and is controlled by the resistance of renal afferent and efferent arterioles. Reductions

ACUTE RESPIRATORY FAILURE

in renal blood flow create a common pathologic pathway for decreasing glomerular filtration rate

(GFR). AKI consists of 3 main mechanisms: prerenal, intrinsic, and obstructive. Acute kidney

injury results from conditions that damage the structures within the kidneys. The most common

form of acute kidney injury causes damage to the parenchyma in the glomeruli, tubules, and

vessels within the kidney. The major causes of acute kidney failure are related to inflammation or

obstruction. This lack of blood flow to the nephrons causes intrarenal necrosis and reduced

glomerular filtration. Acute tubular necrosis is characterized by the destruction of tubular

epithelial cells and acute suppression of renal function due to death of tubular cells. Acute

tubular necrosis due to ischemia and nephrotoxic agents are the most common cause of renal

failure. Since the patient was septic due to Pneumonia, the infectious toxins in the blood stream

sensitized the tubular cells to the damaging effects of tubular necrosis. This exacerbation of

kidney injury caused the patients’ GFR to be 33 ml/min. A normal GFR should be over 60

mL/min. The patient’s kidney injury was also represented by her elevated creatinine level of 1.5

mg/dL. The normal range for blood creatinine is 0.5-1.3 mg/dL. Creatinine is a chemical waste

product that's produced as a result of muscle metabolism. Healthy kidneys filter creatinine from

your blood. The filtered creatinine leaves the body in your urine. If the kidneys aren't functioning

properly, an increased level of creatinine may accumulate in your blood. A serum creatinine test

measures the level of creatinine in the blood and provides an estimate of how well the kidneys

are filtering (Grossman, Disorders of Renal Function and Fluid and Electrolytes, 2014).

Because of the patient’s acute kidney injury, she began to develop uremic

encephalopathy. Uremic encephalopathy is caused by many toxins that accumulate due to acute

kidney failure. Parathyroid hormone likely contributes to uremic encephalopathy which causes

an increase in calcium content in the cerebral cortex. The specific mechanism by which PTH

ACUTE RESPIRATORY FAILURE

causes a disturbance in brain function is unclear, but it may be caused by increases in

intracellular concentration of calcium in brain cells (Grossman, Disorders of Renal Function and

Fluid and Electrolytes, 2014).

Metabolic acidosis is caused by a decrease in plasma HCO3- concentration along with a

decrease in blood pH. In metabolic acidosis, the body attempts to compensate for the decrease in

pH by increasing the respiratory rate. The results in decreased PCO2 levels in the blood which

will lower the blood pH since PCO2 is an acidic molecule. One the main causes for metabolic

acidosis is the inability of the kidneys to excrete the acids produced during normal metabolism.

When the kidneys are functioning normally they conserve HCO3- and secrete H+ ions into the

urine to regulate acid-base balance. In a patient with AKI, there is a loss of both glomerular and

tubular function causing a retention of nitrogenous wastes and metabolic acids. This causes an

imbalance in the patient’s arterial blood gasses creating an acidotic state. The patient’s pH was

7.27 which is acidic. The normal range is 7.38 – 7.42. The patient’s PaCO2 level was 51.8 mm

Hg which is higher than normal limits. The normal range for PaCO2 is 38 - 42 mm Hg. Because

CO2 is an acidic molecule, the build-up of CO2 in the blood stream contributed to the acidosis.

The patient’s acute respiratory failure from the pneumonia, impairs the exchange of CO2,

resulting in a lowered pH. The patient’s HCO3- level was 20.5 mEq/L. This is an alkaline

molecule that is balanced by the kidneys. The normal range for HCO3- is 22 – 28 mEq/L. The

damage to the kidneys from the infection caused and over excretion of bicarbonate, contributing

to metabolic acidosis (Grossman, Disorders of Acid-Base Balance, 2014).

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PICO Question of Patient or Patient Population

P= Patient or population: Patient’s with pneumonia

I = Intervention (something is done): hourly use of incentive spirometer

C= Comparison (there may or may not be a comparison):

O = Outcome (must be measurable): The patients symptoms will improve.

Question: How does the use of an incentive spirometer effect symptoms of pneumonia.

ACUTE RESPIRATORY FAILURE

The II. Medications

Student should also have medication cards or book available on clinical.

Include PRNs that have been administered with the last 24 hours.

Medication

Generic & Trade

Rout

Dosage &

Frequency

Category/Mechanis

m of Action

Contraindications /

Cautions

Side Effects Use for this

patient

Albuterol

(Proventil)

NEBU 3 mg

RTQID

Adrenergic β2-agonist,

sympathomimetic,

bronchodilator; causes

bronchodilation by action

on β2 (pulmonary)

receptors by increasing

levels of cAMP, which

relaxes smooth muscle;

produces bronchodilation,

CNS, cardiac stimulation,

as well as increased

dieresis and gastric acid

secretion; longer acting

than isoproterenol

(Skidmore-Roth, 2011,

p.96)

Hypersensitivity to

sympathomimetics,

tachydysrhythmias, severe

cardiac disease, heart block

(Skidmore-Roth, 2011)

Tremors, anxiety,

restlessness,

bronchospasm

(Skidmore-Roth,

2011)

This is a

broncho

dialator that is

used to

improve the

patient’s

respiratory

function.

Famotidine

(Pepcid)

PO 20 mg/tab

BID

H2-histamine receptor

antagonist; competitively

inhibits histamine at

histamine H2-receptor

site, decreasing gastric

secretion while pepsin

remains at a stable level

(Skidmore-Roth, 2011,

p.485)

Hypersensitivity (Skidmore-

Roth, 2011)

Headache,

dizziness, seizures

in renal disease,

dysrhythmias,

constipation,

thrombocytopenia,

aplastic anemia,

toxic epidermal

necrolysis,

Stevens-Johnson

syndrome,

pneumonia

This is used to

decrease the

patient’s risk of

a GI stress

ulcer.

ACUTE RESPIRATORY FAILURE

(Skidmore-Roth,

2011)

Potassium

Chloride

(Klor-Con)

PO 40 mEq

BID

Electrolyte, mineral

replacement; needed for

adequate transmission of

nerve impulses and

cardiac contraction, renal

function, intracellular ion

maintenance (Skidmore-

Roth, 2011, p.915)

Renal disease (severe), severe

hemolytic disease, Addison’s

disease, hyperkalemia, acute

dehydration, extensive tissue

breakdown (Skidmore-Roth,

2011)

Cardiac depression,

dysrhythmias,

arrest, peaking T

waves, lowered R

and depressed RST,

prolonged P-R

interval, widened

QRS complex,

nausea, vomiting,

cramps, diarrhea

(Skidmore-Roth,

2011)

This is used to

replace the

patient’s

electrolytes

Tramadol

(Ultram)

PO 50 mg/tablet

Daily PRN

Analgesic; not completely

understood, binds to

opioid receptors, inhibits

reuptake of

norepinephrine, serotonin;

does not cause histamine

release or affect heart rate

(Skidmore-Roth, 2011)

Hypersensitivity, acute

intoxication with any CNS

depressant, Pregnancy (C),

breastfeeding, children, geriatric

patients, seizure disorder,

renal/hepatic disease, respiratory

depression, head trauma,

increased intracranial pressure,

acute abdominal condition, drug

abuse (Skidmore-Roth, 2011)

Seizures,

neuroleptic

malignant

syndrome-like

reactions, GI

bleeding,

anaphylaxis,

Stevens-Johnson

syndrome, toxic

epidermal

necrolysis

(Skidmore-Roth,

2011)

This is used to

treat the

patient’s

moderate pain.

Fondaparinux PO 50 mg

Q6PRN

Antithrombotic agent;

inhibits factor Xa, which

interrupts blood

coagulation cascade and

inhibits thrombin

formaiton and thrombus

development; generally

does not increase

Anemia, Fever, Nausea Epidural or spinal

hematomas may

occur in patients

undergoing

anticoagulation

with low-

molecular-weight

heparins (LMWHs)

This is used to

prevent

ACUTE RESPIRATORY FAILURE

prothrombin time (PT) or

partial thromboplastin

time (PTT)

or heparinoids who

receive neuraxial

(epidural or spinal)

anesthesia or spinal

puncture

V. Top Three Prioritized Medical and Nursing Diagnosis

1. Acute Respiratory Failure: Impaired gas exchange RT: Shortness of breath, occasional coughing, excess fluid in the lungs, altered

mental state, pain in the chest, Low oxygen saturation of 91%

2. Acute Kidney Injury: Fluid overload RT: Inability of kidneys to excrete enough fluid AEB: GFR of 33 mL/min, Shortness of breath,

edema, and high blood pressure.

3. Pneumonia: Infection RT: stasis of respiratory secretions AEB: WBC count of 11.9, Shortness of breath, lung pain, weakness.

Care Plan

ACUTE RESPIRATORY FAILURE

Medical & Nursing Dx Nursing Outcomes (NOC) Nursing Interventions (NIC) Evaluation

Acute Respiratory Failure: Risk

for impaired gas exchange RT:

Shortness of breath, occasional

coughing, excess fluid in the

lungs, altered mental state, pain

in the chest, Low oxygen of 91%

1. At the end of the day, the

patient will have a

reduced WBC count

AEB Taking blood labs.

2. At the end of the day, the

patient’s mental status

will improve to oriented

x4 AEB Asking patient

person, place, time, and

task.

1a. Monitor vital signs for an

elevated temperature and

hypotension

Rationale: This will help

identify symptoms of shock.

1b. Perform thorough hand

hygiene when working with the

patient

Rationale: This will reduce the

risk of introducing the patient

to microorganisms

1c. Limit the amount of visitors

Rationale: This will reduce the

patient’s exposure to pathogens.

2a. place a straight catheter as

prescribed.

Rationale: This will relieve

pressure off the patient’s

bladder.

2b. Administer Lasix as

prescribed

Rationale: This will help reduce

intravascular volume.

1. At the end of the day the

patients WBC count was

within normal limits.

2. At the end of the day the

patient was oriented x4

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3. At the end of the day the

patient’s shortness of

breath will resolve AEB

Improving the patient’s

measurement on the

incentive spirometer by

15%.

2c. Maintain strict I and Os

Rationale: This will help track

how much fluid that the patient

is retaining.

3a. Encourage the patient to

cough and deep breathe.

Rationale: This will help

remove mucus from the lungs

and reduce the risk of bacterial

growth.

3b. Encourage patient to use

incentive spirometer.

Rationale: This will help them

track their progress and

encourage them to cough and

deep breathe.

3c. Educate the patient on the

importance removing static

mucus from the alveoli.

Rationale: This will help them

understand the reason for using

the incentive spirometer.

3. At the end of the day the

patient did not complain

of shortness of breath.

References

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Grossman, S., & Porth, C. (2014). Disorders of Ventilation and Gas Exchange. In D. Troy (Ed.), Porth's Pathophysiology (9th ed., pp. 958-

991). Philadelphia: Wolters Kluwer Health.

Grossman, S., & Porth, C. (2014). Disorders of Renal Function. In D. Troy (Ed.), Porth's Pathophysiology (9th ed., pp. 1083-1109).

Philadelphia: Wolters Kluwer Health.

Grossman, S., & Porth, C. (2014). Disorders of Acid Base Balance. In D. Troy (Ed.), Porth's Pathophysiology (9th ed., pp. 1074-1075).

Philadelphia: Wolters Kluwer Health.

Grossman, S., & Porth, C. (2014). Disorders of Renal Function and Fluids and Electrolytes. In D. Troy (Ed.), Porth's Pathophysiology (9th ed.,

pp. 998-1148). Philadelphia: Wolters Kluwer Health.

Devarajan, V. R. (2016, February 16). Haemophilus Influenzae Infections. Retrieved April 10, 2017, from

http://emedicine.medscape.com/article/218271-overview?

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%3D#a6

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