OSAHS + OHS + ARDS

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6 Terms

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Obstructive Sleep Apnea-Hypopnea Syndrome (OSAHS)

Recurrent episodes of PARTIAL or COMPLETE (narrowing/COLLAPSE) pharynx/airway obstruction during SLEEP --> Recurrent AWAKENINGS or AROUSALS to re-establish airway patency

-ONLY experience occlusion during INSPIRATION (Exerts negative pharyngeal pressure and reduces the tone of the genioglossus muscle)

-Underdx

-Mostly asymp

-Have a lot of comorbidities

Risk Factors (precipitate or worsen):

•Obese middle aged man

•Older age

-African American gets affected more regardless of age (younger than usual)

•OBESITY --> thick neck

•ETOH or sedative drugs --> can't wake up at night to breath

•NASAL OBSTRUCTION

•Smoking

•Genetics

•CRANIOFACIAL and upper airway soft tissue ABNORMALITIES + Fat deposition --> Upper airway size is SMALLER

Types:

•HYPOpnea: REDUCTION in airflow

-10-second event during which breathing CONTINUES BUT

-Ventilation during sleep is REDUCED at least 50% from baseline (gas exchange)

•Apnea: COMPLETE CESSATION of airflow

-Cessation >_ 10 seconds

Types:

•OBSTRUCTIVE apnea: cessation of airflow but with continued RESPIRATORY EFFORT (trying to breathe/using muscle)

-Usually have HF or stroke

•CENTRAL apnea: airflow and respiratory effort are both ABSENT

Symptoms:

•MC: SLEEPINESS* and daytime somnolence

•Poor concentration

•Daytime fatigue

•Unrefreshing sleep

•NOCTURNAL CHOKING or gasping

•Nocturia (due to false signal of fluid overload due to hypoxia [acidic blood])

•Depression and decreased libido

•Bed partners* report:

-SNORING*, apneas, RESTLESS sleep, or irritability

*3 S's

Signs:

•Narrow or "CROWDED" oropharynx

-Mallampati 3 or 4 (limited visibility of hard or soft palate)

-Macroglossia

-Tonsillar enlargement

-Narrow palate

•HYPERTENSION

•LOWER LIMB EDEMA

•Obesity (High BMI)

•LARGE neck circumference

•Craniofacial abnormalities

-Retrognathia (mandible is positioned further back than the upper jaw)

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OSAHS Dx + Severity + Tx

Dx:

•Questionnaires

-The Epworth Sleepiness Scale

-STOP-BANG

•Labs

-Secondary polycythemia (hypoxic)

-Proteinuria

-Hypothyroidism

-Hypercapnia (high CO2)

-Low PO2

•NOCTURNAL CARDIAC ARRHYTHMIA

•Polysomnography (GOLD STANDARD)

-Night-to-night variability --> Misdx ESP in MILD cases

--Negative first-night test is INSUFFICIENT to rule out OSAHS w/ HIGH SUS --> Retest in lab if possible

-Home vs Lab

•Apnea Hypopnea Index (AHI)

-# of times Pt experience Hypo or Apnea during sleep (measures the severity)

-Asymp: >_15/hour

-Symp or w/ comorbidities: >_5

Severity:

•Mild: b/w 5-14 respiratory events per hour of sleep

•Moderate: b/w 15-30 respiratory events per hour of sleep

•Severe: > 30 respiratory events per hour of sleep

Tx:

-Lifestyle:

•No Etoh or hypnotics

•Wt loss (i.e GLP-1 agonists like ozempic)

-Devices:

•Nasal continuous positive airway pressure (CPAP)*

•Oral appliances (reposition oropharynx to keep it open)

•Hypoglossal nerve stimulation (INSPIRE)

-Like a pacemaker

-Stabilize Pt's throat --> Prevent obstruction

-Components: Neurostimulator, Pressure sensing lead, Stimulator lead

•Stimulant drugs (not rec)

•Surgical procedures (only if it can be fixed i.e enlarged tongue)

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Obesity Hypoventilation Syndrome (Pickwickian syndrome)

Presence of AWAKE alveolar HYPOventilation (PaCO2 ≥45 mmHg) in obese individual (BMI ≥30 kg/m2), which CANNOT be attributed to other conditions associated with hypoventilation

Clinical Presentations:

•Airway:

-Severe upper airway OBSTRUCTION

-OSA

•Respiratory:

-Restrictive chest physiology

-Pulmonary hypertension

-Hypoxemia/Hypercapnia

•Cardiovascular:

-CAD

-CHF

•CNS:

-BLUNTED CENTRAL RESPIRATORY DRIVE (Normal: High CO2 detected in brain --> stimulate breathing)

•Others:

-Diff vascular access

-Diff positioning

DISTINCT from obesity + OSA

Dx:

*EXCLUDE EVERYTHING FIRST

•PFT

-Chronic RESPIRATORY ACIDOSIS (PaCO2 ≥45 mmHg) with compensatory metabolic alkalosis

*Important to assess for Pt undergoing surgery

*Assess + tx complications

Tx:

•CPAP

-Improves:

-Gas exchange

-Lung volumes

-Sleep-disordered breathing

-Reduces mortality

•Weight loss

-Bariatric surgery

-GLP-1

•If FAILS, options include:

-Tracheostomy

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Acute Respiratory Distress Syndrome (ARDS)

Acute hypoxemic respiratory failure following a systemic or pulmonary insult W/O evidence of HF (no effusions, cardiomegaly, venous engorgement in upper lung zones, indistinct blood vessels)

-Physiologic + Radiographic Syndrome

Patho:

•Pro-inflammatory cytokines --> lung injury:

-Damage to capillary endothelial cells --> Increased vascular permeability --> Increase fluid in alveoli --> Damage/collapse alveolar epithelial cells --> Decreased production and activity of surfactant:

-->

-Interstitial + alveolar pulmonary edema

-Alveolar collapse

-Hypoxemia

--> NO GAS EXCHANGE

Risk Factors:

-SEPSIS (1/3 of pts)

-Severe MULTIPLE TRAUMA

-ASPIRATION of gastric contents

-Shock

-Infection

-Lung contusion

-Non-thoracic trauma

-Toxic inhalation

-Near-drowning

-Multiple blood transfusions

-Drugs

Dx:

*MUST EXCLUDE Cardiogenic Pulmonary Edema (HF)

•Clinical

-Rapid onset of profound dyspnea:

--Labored breathing

--Tachypnea

--Intercostal retractions

-Frothy RED or PINK sputum

-DIFFUSE CRACKLES

-MULTIPLE ORGAN FAILURE

-MARKED HYPOXEMIA (refractory to supp O2)

•CXR (normal first)

-Peripheral BILATERAL INFILTRATES (white out)

--Diffuse or Patchy

--Infiltrates rapidly become CONFLUENT

-AIR BRONCHOGRAMS

-Normal Heart size

-Small or nonexistent Pleural Effusions --> SPARE COSTOPHRENIC ANGLES

•Pulmonary capillary wedge pressure

-NORMAL: ≤ 18 mm Hg

-Measure the L ventricular filling pressure (heart fx)

•PaO2/FIO2 ratio <300

-Arterial oxygen over amount of oxygen giving (put to decimal)

-Normal: 400-500

*PRACTICE CALC

PaO2/FIO2 ratio Severity:

•Mild: b/w 200-300 mm Hg

•Moderate: b/w 100-200 mm Hg

•Severe: <100 mm Hg

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ARDS Tx + Prognosis

Tx:

•Identify + tx underlying precipitating and secondary conditions (i.e sepsis)

•Tracheal intubation

•Positive end expiratory pressure (PEEP) mechanical ventilation

-Revive (recruits) atelectatic alveoli

-LOWEST levels + Supplemental oxygen:

--PaO2 >55 mm Hg or the SaO2 above 88%

•O2:

-Efforts should be made to DECREASE FIO2 to less than 60% ASAP --> AVOID oxygen toxicity

-SAFE: <40%

•GOAL of fluid management:

-Maintain pulmonary capillary wedge pressure at the LOWEST level compatible with ADEQUATE cardiac output

Prognosis:

-High Mortality

-2 weeks survival

-Survivors have lots of complications

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