comple concepts in respiratory function and alterations

upper airway structures

• nose, sinuses and nasal passages, pharyn, tonsils and adenoids, and laryn, which warrm, humidifiy, and filter atmospheric air

• laryn connects the pharyn and the trachea, laryn has the epiglottis that helps with the aspiration

lower respiratory tract

• includes the trachea, mainstem, and secondary bronchi, bronchioles, and lungs

how does respiration work

• process of respiration requires gas ehanche in both lungs, termed eternal or pulmonary respiration, and ultimatelly, in the tissues, termed internal or cellular respiration

• venitlation: just inspiration and epiration, mechanics of ventilation can impact this

• diffusion: o2 and CO2 travel across the alveolar-capillary membrane

• perfusion: blood flow through the pulmonary circulation

• other jobs of the respiratory system:

  • Controlled by medulla oblongota and pons, adjusting ventilations based on PCO2 and pH levels

    • Lungs echange CO2 for O2 while kidneys secretes bicarbonate to maintain a PH between 7.35 and 7.45

    • fluid balance waters is removed during epiration

how it all works

• oygen diffuses across the alveolar-capillary membrane from thr alveoli, where the oygen partial pressure is higher, into the pulmonary capillary where the oygen partial pressure is lower

• oygen is transported in the blood in two ways:

  • About 98% binds to hemoglobin in rbcs

  • about 2% is dissolved directly in the plasma

• carbon dioide is transported by the blood from the tissues back to the lungs. in the lungs, CO2 diffuses from the pulmonary capillary blood, where its partial pressure is higher, into the alveoli, where its partial pressyre is lower, it is then removed from the body when we ehale

• oygen moves from the alveoli into the blood, while carbon dioide moves from the blood into the alveoli

• how do we know oygenation is adequate

  • PaO2: normal arterial oygen pressure is about 80-100 mmHg (some labs use 80-85)

  • pulse oimetry (SpO2): usually 95-100% in healthy adults: many clinicians consider >93% acceptable depending on the patient

v/q imbalance or mismatch

• occurs as a result of inadequate ventilation, inadequate perfusion, or both

• both shunting and dead space can lead to hypoia/hypoemia

V/Q imbalance or mismatch: shunting

• venitlation is absent or severely impaired in an area of the luung, while perfusion remains adequate. as a result, blood passes trough the pulmonary capillaries without being adequately oygenated (pneumonia, tumor)

V/Q imbalance or mismatch: deadspace

• occurs when air reaches the alveoli, but there is little or no blood flow to pick up the oygen or removed carbon dioide (typically a PE)

what is hypoia

• low levels of cellular oygen

• us when the bodys tissues do not receive or cannot use enough oygen to function properly

• presentation: change in mental status, aniety, restlessness, and/or confusion, dyspnea, tachycardia, and tachypneic, SOB

• causes: PE, anemia, trauma, shock

what is hypoemia

• low levels of oygen in the arterial blood

• pAO2 < 60 mmHg or SaO2 < 90% on RA

• May persist even with sypplemental O2

• Hypoemia is often a primary cause of hypoia

initial assessment

• chief complaint: why are you here? (What clinical manifestations), acute vs chhronic

• factors that improve or worsen symptoms (movement, pain, cough)

• patient history PMH, social factors, family, recent travel, smoking status, occupation, ADLs

• physical markers: look at weight

• safety: medications, allergies

physical assessment

• inspection: look at speech, use of accesory muscle, orientation, and aniety level

• clinical signs: dyspnea (SOB), Cough, sputum production, chest pain, wheezing, clubbing, abd hemoptysis

• chronic indicators: clubbing and barrel chest

• vitals: pulseo and respirations (monitoring for fast, slow, absent, or retractions)

• palpatation and percussion: limited palpation for crepitus; percussion is generally not performed

• auscultation: evaluation of normal lung sounds

where should i put my stethoscope?

• bronchial: neck and trachea

• bronchovesicular: first to second intercostal spaces

• vesicular: below the second intercostal space and peripheral lung fields

what will you do first?

• cardiac monitor: pulseo, lookk at waveform

• oygen: assess immediate need

• labs: including ABGs and d-dimer

• Capnography: consider end tidal CO2

• imaging and samples: chest -ray and sputum

diagnosis for later

• chest -ray

• CT-CTA scan

• MRI/PET

• VQ scan

• pulmonary

indications for oygen

• the goal of using therapy is to prevent or correct tissue hypoia, which is decr. oygen supply

• oygen transport to the tissue is dependent not only on the arterial oygen content but also on cardiac output, hemoglobin concentration, and metabolic requirement

• each system and oygen flow rate is designed to procide a specific fraction of inspired oygen (FiO2), perentage of oygen, or liters per minute (L/min). The appropriate form of oygen therapy is best determined by ABG levels, which indicate the patients oygenation status (PO and/or PaO2)

remember to assess your patients when applying oygen

• phsyical assessment

• what do they look like?

• vitals (pulseo)

• Labs (ABGs)

• do they need oygen (Acute vs chronic)

• 93% pulse o of below

tpes of oygen management: low flow mied with air

• nasal cannula (1-6 liters)

• simple face mask (5-10 liters)

• partial rebreather (8-10 liters)

• non rebreather (12-15)

tpes of oygen management: high flow: provide set oygen concentration regardless of breathing patterns

• venturi mask (2-15 L)

• aerosol mask (humidification and/or meds)

• tacheostomy collar (high)

• t-piece adaptor (etubation)

• face tent

• vapotherm (up to 60 L/min) blended with compressed air

complications of oygen therapy

• oygen toicity: develops from concentrations >50% oer 24-48 hrs. Use the lowest effectice dose

• mucous membrane dryness: common side effects requiring monitoring

• infection risk associated with therapy equipment

invasice airway management

• emergency care:

  • endotracheal (ETT) tube is the standard for immediate airways access. RN assisted with intubation in critical care areas? What do we do?

• LLong term care

  • tracheotomy is preferred for patients requiring etended ventilation support

• duration

  • airway management solutions are selected based on whether the need is temporary or long term

what is your role as a nurse during intubation?

• continuous monitoring of patient (cardiac monitor, vital signs)

• assist the HCP (set up, bagging, sunctioning, sedation, capnography)

• look at the rise of the chest, end-tidal Co2

• assessment (breath sounds, chest movement)

• chest ray (tube placement)

• documentation (where is it? moving)

• communication

now what do i do since they are on a vent?

• full head to toe assessment (comple resp. assessment, neuro, skin)

• continuous monitoring (vitals, cardiac monitor)

• sedation

• suctioning

• repositioning

• tube feedings

• move ET tube per protocol

complications of mechanical ventilation

• unplanned etubation

• aspiratioon (HOB >30)

• Infection: Ventilator acquired pneumonia (antibiotics, frequent mouth care)

• hypotension

• barotrauma

if i need to be on a vent, long term

• tracheostomy may be either teporary or premanent

• repaces the ET tube

• cuffed or uncuffed

what is my nursing care for a trach patient

• suction look at policy (based on assessment)

• suctioning (<15 secs, waiting at least 1 minute between suctioning events)

• good resp. assessment

• look at vital signs

• good positioning (semi-fowlers)

• provide trach care (cuffed, make sure there is air)

• communication

• if trach tube fell out = decannulation(you need a trach set and intubtion set up)

what is atelectasis

• collapse of alveoli, leading to the loss of lung volume

• classificated by its cause

• alveoli must remain open for gas echange. collapse happens when ventilation is lsot, preventing fresh air from replenishing oygen and allowing carbon dioied to accumulate

• the collapsed alveoli cannot ventilate preoper, so oygen cannot enter the blood effectively in that area. if blood continue flowing past them, a shunt-like effect occur

• mechanical obstruction: airway secretion, mucus plugs, froeign bodies, bronchial tumors, or oygen toicity

• clinical conditions: ARDS, pleural effusions, and lung tumors

risk factors and diagnosis for atelectasis

• RF: post op pts, chronic lung diesease, morbid obesity, CVA

• diagnosis: chest -ray, followed by CT scan and maybe ultrasound, later: bronchoscopy

  • need an ABG

s/s of atelectasis

• dyspnea, sough, sputum production, and leukocytosis (elevated WBC)

• crackles, decr/diminsihed breath sounds; wheezing/stridor (if obstruction is the cause)

• if large enough can cause develop significant resp. distress (can be a problem)

treatment and prevention of atelectasis

• treatment: O2, bronchodilators, CPT, mucolytic agents (Acetylcysteine mucomyst)

• prevention: primary measure is incentive spirometry, education of pts

pulmonary edema what is it?

• abnormal accumulation of fluid within the lung tissue, the alveolar space, or both

• can be life threatening (if it is acute “flash”

• types:

  • cardiogenic or noncardiogenic (e.g. ARDS - most common cause)

• capillary fluid leaks or is forced by high hydrostatic pressure into alveolar space (they dont work, causing intrapulmonary shunting of blood and hypoemia)

s/s of pulmonary edema

• resp. distress: incr. distress chractaerized by dyspnea, air hunger, and hypoemia

• aniety and agitation: patients are typically very anioy sand frequently agitated

• foam/froth: formed as fluids leaks into alveoli and mied with air (more common in cardiogenic edema), pink tinged frothy sputum

pulmonary edema assessment and treatment

• assess: may present with distinct crackles or wheezing

• treat:

  • oygen therapy: administer oygen as rquired, may need to be intubated

  • underlying cause: identify and aggresively treat the underlying pathology

what is pleurisy

• pleyrisy refers to inflammation of botth layers of the pleurae (parietal and visceral)

• it is with something else

assessment and treatment of pleurisy

• sharp knife like pain, stabbing, worsens with deep breath, coughing, or sneezing or movement, on one side

• auscultaiton: pleural friction rub may be heard

• etiology: found with pneumonia, infection, trauma, PE, or cancer

• treatment: positioning, NSAIDs, lidocaine patches, side lyinh

what is pleural effusion and its causes

• a collection of fluid in the pleural space

• too much fluid and it can be infection

• complicaiton of HF, TB, pneumonia, PE, or tumors

what is empyema

• An accumulation of thick, purulent fluid (PUS) within the pleural space. cause is usually strep (pneumonia) A. form of pleural effusion

• what does pleural effusion and empyeme present as

• SOB, resp. distress

• decr. breath sounds

• empyeme; acutely ill, fever, chills, pain, cough, tachycardia

• depends on how much, if it is infectious, what is the cause

treatment and diagnosis of pleural effusion and empyema

• physical eam, chest -ray, CT scan, ultrasound, thoracentesis

• treatmnet:

  • treat the underlie cause

  • prevent fluid accumulation

  • relieve discomfort and resp. compromise

acute resp. failure what is it

• sudden and life threatening deterioration of the gas echange function of the lung

• echange of oygen for carbon dioide in the lungs cannot keep up the rate of oygen consumption and carbon dioide producion by the cells of the body

• ventilation or perfusion mechs in lung are impaired, impairs sstems lead to ARF include: problems with ventilation, diffusion, and perfusion, can have VQ mismatch

• common causes of ARF can be classified into 4 categories: decr. resp. drive, dysfunction of the chest wall, dysfunction of the lung parenchyma, and other causes

acute resp. failure 2 diff classifications

• 2 types:

  • hypocemic: PaO2 < 50 mmHg on room air OR

  • hypercapnic:: PaCO2 > 50 mmHg with a Arterial pH < 7.35

what does acute. resp. failure look like or caused by

• decr. resp drive: brain injuries, trauma, oversedation, drug overdose

• dysfunction of the chest wall: neuromuscular, spinal cord injury

• dysfunction of the lung parenchyma: pneumonia, PE

• others: major surgeries

clinical manifestations of acute resp. failure

• restlessness, fatigue, headache, dysppnea, air hunger, mild tachycardia and tachypnea, and incr. BP

• more obvious signs may be present, including confusion, lethargy, incr. tachycardia, tachypnea, central cyanosis, diaphoresis, and finally resp. arrest

• manifestiona sare usually related to hypoemia, hypercapnia, and acidosis

• objectives: correct underlying cause and restore adequate gas ehange in the lungs

how to diagnose and treat acute. resp. failure

• ABGs, VBGs, CBC, sputume culture, BMP

• Ct scan

• what is underlying and what you need to treat (resp. fail is caused by something)

• oygenation

• may need ventilator (PEEP)

• meds:

  • inhaled bronchodilators

  • steroids

  • diuretics

  • antibiotcs

what is acute resp. distress syndrome

• acute lung injury

• characterized by a sudden and progressive pulm. edema, incr bilateral infiltrates on chest ray, hypoemia refractory to supplemental oygen, and reduced lung compliance

• nonfunctioning alveoli, and gas echange is markedly imapired, resulting in seere, refractory hypoeemia (they have to be intrubated)

• this can lead to organ failure if not treated promptly and effectively. can lead to MODS

• make sure it is not HF

patho of ARDS

• triggered by direct pulm. insults (such as severe pneumonia, aspiration, or inhalation injury)

• indirect such as sepsis, severe trauma, or pancreatitis

• signs: acute onset of dyspnea about 12-48 hrs after an event, u see use of acessory muscles, crackles, pink frothy sputum

• arterial hypoemia that does not respond to oygen

• ARDs occurs as a result of an inflam. trigger that initiates the release of cellular and chemical mediators, causing diffuse epithelial cell injury to the alveolar capillary membrane

• leakage of protein rich fluid blood cells into the alveolar insterstitial spaces and alterations in the capillar beds

diagnosis of ARDS

• chest ray (look for bilateral infiltrate)

• CT scan

• Labs ABGs, CBC, BPM, coagu;ation panel, CRP, liver and renal

• urine

• sputum

• mmay need echo

treatment and support for ARDS

• mechanical ventilation with PEEP

• hemodynamic stability

• proning

• fluids

• tube feedings

• meds:

  • antibiotics

  • diuretics

ARDS complications

• Ventilator-Associated pneumonia

• barotauma

• stress ulcers

• renal failure

• MODS: the primary cause of death in ARDS, often accompanied by sepsis

• 40% of patients with ARDS die

definition and RF pulmonary embolism

• obstruction of one or more branches of the pulm. arteries

• usually a thombus but can be other

• biggest RF: DVT

• smoking, obesit, surgery, birth control

• A-fib, surgery, ppregnancy, and HF

pulmonary embolism patho

• obstructionion leads to an impaired ventilation to perfusion ratio (V/Q mismatch)

• decr. blood flow to alveoli leads to hypoemia. Alveoli are ventilated but not perfused

• can have a lot of issues

• different classificantion of PEs

PE clinical manifestations and diagnosis

• the sudden onset of intense dyspnea, pleuritic chest pain, cough and tachypnea

• tachycardia

• aniety

• pain in a leg

• dizziness

• may have hemooptysis

• blood draw (CBC, cardiac enzymes, D-dimer, DNP, ABG)

• chest ray

• ekg/ecg

• may do an ultrasound

later:

• CT scan (PE), MRI, VQ Scan, Pulmonary angriography

how do you treat a patient with a PE?

• Anticoagulation

  • Low-molecular-weight hepain (LMWH)

  • IV hepain

  • warfarin (COumadin)

  • Novel oral anticoagulants such as apiaban and rivaroaban (factor a inhibitors)

• Fibrinolytic agents (only if patient is compromised)

  • tissue plasminogen activator (tPA)

  • alteplase (Activase)

• Surgery

• Embolectomy

occupational lung disease

• diseases of lungs occur in numerous occupations a sesult of eposure to several different types of agent

• one category of occupational lung disease that causes chronic fibrotic lung disease is pneumoconiosis, which is caused by inhalation of inert, inorganic, or silica dusts

• most common types of pneumoconiosis are coal workers pneumoconiosis, silicosis, and asbestosis

• patho of each type of pneumoconiosis (any chronic lung disease caused by the inhalation of particles) begins with the inhalation and deposition of industrial dusts ir particles in the lungs

clinical manifestations and assessment: silicosis

• present with: dyspnea, fever, cough, weight loss

• note: rapid disease progression. progressive massive fibrosis

• treatment: limited to supportive care. fibrotic process is irreversible.

clinical manifestations and assessment: asbestosis

• symptoms:: progressive dyspnea, persistent dry cough

• early findings: bibasilar fine end-inspiratory crackles

• advanced cases: clubbing of the fingers

• treatment: limited to supportive care. fibrotic process is irreversible.

what is an ABG?

• acid/base balance reflects hydrogen ions

• ability of the lungs to provide adequate O2 and remove CO2 (bentilation)

• ability of the kidneys to reabsorb or ecrete bicarb (HCO3) to maintain normal body pH (metabolic state)

• specimen obtained from radial, brachial or femoral artery, or an arterial line

• complications: pain, hematoma, hemorrhage

respiratory acidosis

respiratory alkalosis

metabolic acidosis

metabolic alkalosis

acidosis/alkalosis