Week 4 3271- Respiratory alterations

Respiratory system structures

upper airways, lower airways, lungs, alveoli (air sacs)

primary role: gas exchange

Respiratory system essential functions

oxygenate tissues (deliver O2), remove CO2, support ventilation/perfusion

Oxygen IN, CO2 OUT ; impaired gas exchange can decrease O2 and increase CO2

Upper respiratory system

nose, sinuses, oropharynx, larynx

main nursing priority: airway patency

Lower respiratory system

trachea, bronchi, bronchioles, alveolar ducts, alveoli, lungs, accessory muscles

main nursing priority: gas exchange

Oxygenation and ventilation

2 separate physiologic processes

Oxygenation: process of getting O2 into the body

Ventilation: process of eliminating CO2 from the body

Hypercapnia

elevated CO2 in the blood (PaCO2 >45mmHg) caused by inadequate ventilation leading to CO2 retention

S/s of hypercapnia

respiratory acidosis, confusion, decreased LOC, SOB, tachypnea

CO2 retention affects brain first: think confusion + drowsiness = check CO2

Hypoxemia

low blood oxygen; low PaO2 in arterial blood

occurs when the lungs cannot affectively oxygenate the blood

Hypoxemia key symptoms

cyanosis (late sign), SOB, confusion

hypoxemia = O2 problem, look for low SpO2 and signs of inadequate O2 delivery

present in blood sample

Hypoxemia nursing priorities

assess SpO2, monitor respiratory status, administer O2 as ordered, identify cause of impaired oxygenation

Hypoxemia vs Hypercapnia

hypoxemia (oxygen problem): low O2--> low SpO2, anxiety/restless/tachy, cyanosis --> improve oxygenation

hypercapnia (ventilation problem): high CO2 --> respiratory acidosis, drowsy/HA/confused --> improve ventilation

Pneumonia

infection of the lungs causing inflammation and fluid-filled alveoli

due to impaired gas exchange and decreased oxygenation

watch for hypoxemia (fluid/WBC fill alveoli --> less O2 in/less CO2 out (aka impaired gas exchange) --> less O2 reaching tissues)

Pneumonia s/s

productive cough, SOB, crackles, fever, hypoxemia (low SpO2), fatigue, chest discomfort, tachypnea

Pneumonia nursing priorities

Assess SpO2 , encourage cough/deep breathing/incentive spirometry, administer antibiotics and oxygen as prescribed, monitor breath sounds, adequate hydration

Focused respiratory assessment

Inspect (increased work of breathing, accessory muscle use, decreased chest expansion)

Auscultate (crackles/wheezes)

Palpate/Percuss (increased tactile fremitus/dullness to percussion)

Pneumonia diagnostic tests

-Chest xray: confirms pneumonia (confirms infiltrates/consolidation)

-Sputum culture: identifies pathogen (identifies the causative organism; obtain before antibiotics if possible)

-ABG & Labs: assess oxygenation (evaluate oxygenation; CBC: elevated WBC may indicate infection; detects hypoxemia)

Community acquired pneumonia (CAP)

acute infection acquired within the community

Hospital acquired pneumonia (HCAP or noscomial)

onset/diagnosis of pneumonia ≥48 hours after admission to hospital

Ventilator-associated pneumonia (VAP or Noscomial)

onset/diagnosis of pneumonia ≥ 48 hours after endotracheal intubation

Pneumonia nursing role

education (vaccines, risk factors, controlled coughing, incentive spirometry, hydration, meds)

strict hand hygiene

apply O2 as prescribed

monitor VS/SpO2

screen for sepsis

Covid-19

viral infection spread through respiratory droplets when an infected individual coughs, sneezes, or talks

SARS-CoV-2 (COVID-19) symptoms

common: chills, muscle or body aches, loss of taste or smell, congestion or runny nose (fever, cough, SOB, fatigue, HA, sore throat, n/v, diarrhea)

severe: trouble breathing, persistent pain or pressure in the chest, new confusion, decreased LOC, cyanosis

Covid physical assessment

general appearance, VS, lung sounds

onset and duration of symptoms

Covid diagnostics

nasopharyngeal swab

oropharyngeal swab

serology (blood)

chest x ray

molecular test: RT-PCR most sensitive in detecting SARS-CoV-2

Quarantine for Covid-19

not up to date with vaccines: quarantine for 5 days, mask, no traveling, test 5 days after exposure (even if no symptoms)

up to date with vaccines: no quarantine, test 5 days after exposure (even if no symptoms)

Isolation for Covid-19

symptoms or positive test: stay home for 5 days, wear mask, no traveling

ending isolation: after 5 full days if fever free for 24 hours (without use of antipyretics); if very sick or altered immunity, isolate for at least 10 days

Pulmonary artery hypertension (PAH)

high pressure in pulmonary arteries

increases workload of right ventricle

can lead to right sided HF

PAH = increased pulmonary pressure --> right ventricular strain --> right sided HF

Pulmonary artery hypertension (PAH) common symptoms

dyspnea on exertion, fatigue, chest pain, syncope, peripheral edema

Pulmonary artery hypertension (PAH) nursing priorities

monitor SpO2 and VS

assess for worsening dyspnea

administer oxygen as prescribed

monitor for right sided HF signs

Pulmonary artery hypertension (PAH) causes

idiopathic (unknown cause)

heritable/genetic mutations

connective tissue disease (scleroderma)

congenital heart disease

drug/toxin associated

HIV, portal HTN, other associated conditions

Pulmonary artery hypertension (PAH) Assessment/Evaluation

Suspected PAH should be confirmed with right heart catheterization after noninvasive assessment

1. Symptoms: exertional dyspnea, fatigue, chest pain, syncope

2. Physical exam: RV heave, loud P2, edema

3. labs: BNP/NT-proBNP, autoimmune testing

4. Echocardiogram: initial screening test

5. ECG, chest xray, PFTs, CT/MRI

6. 6 minute walk test and functional class

***7. Right heart catheterization = diagnostic gold standard***

Pulmonary artery hypertension (PAH) manifestations

dyspnea, fatigue, weakness, chest pain, dizziness, syncope

advanced: hemoptysis, hoarseness, eventual RHF, ascites, edema, liver enlargement, increased jugular venous pressure

end stages: cyanosis

Pulmonary artery hypertension (PAH) management

pharmacologic therapy: diruretics, oxygen, anticoagulants, calcium channel blockers, sildenafil

try to dilate blood vessels

Acid-base balance

homeostatic mechanisms keep pH within normal range (7.35-7.45)

buffer systems (prevents major changes in pH, carbonic acid-bicarbonate system)

lungs (regulate CO2)

kidneys (regulate bicarbonate levels)

Hydrogen ions in acid-base balance

must be maintained in a narrow range; expressed as pH (1-14; 7 is neutral); number of H+ in body fluid determines if its acidic, alkaline, or neutral (pH: 7.35-7.45)

acids: produced as end products of metabolism; contains H+

bases: does not contain H+

pH

hydrogen ion concentration

range: 7.35-7.45

Hypo/<7.35: acidosis

Hyper/>7.45: alkalosis

PaCO2

partial pressure of carbon dioxide in arterial blood

range: 35-45 mmHg

Hypo/<35: respiratory alkalosis

Hyper/>45: respiratory acidosis

PaO2

partial pressure of oxygen in arterial blood

range: 80-100 mmHg

Hypo: <80 = mild hypoxemia, <60 = mod hypoxemia, <40 = severe hypoxemia

Hyper: >100mmHg = hyperoxygenation

HCO3-

bicarbonate

range: 22-26 mEq/L

Hypo/<22: metabolic acidosis

Hyper/>26: metabolic alkalosis

Respiratory acidosis

low pH (<7.35), HIGH CO2 (PaCO2 > 45 mmHg), normal or high HCO3-

too much carbonic acid from HYPOVENTILATION

ROME (Respiratory, Opposite, Metabolic, Equal)

Respiratory Alkalosis

high pH (>7.45), LOW CO2 (PaCO2 <35 mmHg), normal or low HCO3-

too little carbonic acid from HYPERVENTILATION

ROME (Respiratory, Opposite, Metabolic, Equal)

Respiratory acidosis causes

HYPOventilation (low pH (<7.35), HIGH CO2 (PaCO2 > 45 mmHg)

airway obstruction, OSA, neuromuscular disease, CNS malfunction (injury to brainstem), drug-induced hypoventilation, respiratory muscle fatigue, high flow oxygen to patient with chronic hypercapnia (COPD), severe pneumonia, ARDS

Respiratory alkalosis causes

HYPERventilation (high pH (>7.45), LOW CO2 (PaCO2 <35 mmHg)

anxiety, PE, sepsis, hypoxia, physiologic response to metabolic acidosis and increased demand, CNS overstimulation (stroke, TBI, meningitis, encephalitis), liver failure, mechanical hyperventilation

Metabolic acidosis

non respiratory acidosis; LOW pH (<7.35), LOW HCO3-, normal or low PaCO2

ROME (Respiratory, Opposite, Metabolic, Equal)

Metabolic alkalosis

non respiratory alkalosis; HIGH pH (>7.45), HIGH HCO3-, normal or increased PaCO2

ROME (Respiratory, Opposite, Metabolic, Equal)

Metabolic acidosis causes

increase in acid (pH< 7.2) or loss of bicarb

ketoacidosis, lactic acidosis, renal failure, intoxication, diarrhea,

may develop Kussmaul respiration (cardinal feature of severe metabolic acidosis)

Metabolic alkalosis causes

decrease in acid (high pH) or increase in bicarb

vomiting, NG suctioning, diuretics, hypokalemia, excess bicarb intake, steroid therapy

Acidosis symptoms

HA, sleepy, confusion, loss of consciousness, coma

SOB, cough

arrhythmia, increased HR

seizures, weakness

n/v, diarrhea

Alkalosis symptoms

confusion, light headed, stupor, coma

hand tremor, numbness/tingling in face, hands, or feet

twitching, prolonged spasms

n/v

ABG interpretation

pH 7.35-7.45

PaCO2 35-45 mmHg

PaO2 80-100 mmHg

HCO3 22-26 mEq/L

ROME- Respiratory Opposite Metabolic Equal

Lungs in ABG balance

respiratory control (fast); acid control; control the level of CO2 (PaCO2) in the blood

CO2 is acidic --> the more CO2, the lower the pH (acidosis)

Kidneys in ABG balance

metabolic control (slow); base control; control the level of HCO3- (bicarb)

low pH (acidosis --> kidneys hold onto more HCO3- (base) and excrete H+ (acid)

Respiratory acidosis/alkalosis compensation

acidosis: kidneys retain HCO3-

alkalosis: kidneys excrete HCO3-

Metabolic acidosis/alkalosis compensation

acidosis: lungs blow off CO2

alkalosis: lungs retain CO2

Uncompensated

pH abnormal + only one of PaCO₂ OR HCO₃⁻abnormal

If the pH is still abnormal, compensation isn't finished.

Partially

compensated

pH abnormal + both PaCO₂ and HCO₃⁻ abnormal

Fully

compensated

pH normal + both PaCO₂ and HCO₃⁻ abnormal

Steps to analyzing

1. Start with pH: Acidosis vs. Alkalosis (range 7.35-7.45)

2. Assess CO2: high, low, or normal (range: 35-45)

3. Assess HCO3: High, low, or normal (range: 22-26)

4. Metabolic or Respiratory? (if CO2 high: respiratory acidosis, if low: respiratory alkalosis ; if HCO3 low: metabolic acidosis, if high: metabolic alkalosis)

5. Assess compensation (comp: pH norm, both abnorm; uncomp: pH abnorm, one abnorm; partial: everything abnorm)

6. Assess oxygenation (≥80 is normal, 60-79 mild, 40-59 moderate, <40 is severe)

Venous vs arterial sammple

look at PaO2 and SaO2:

levels extremely low in venous blood sample, so arterial sample (ABG) used to look at oxygen saturation

VBG may be used to assess pH and acid-base status (ex: in a patient with DKA)

if results don't match the patient presentation, redraw the ABG