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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)
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)
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
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
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