Pulm. OSA and OHS + mehlham (09-29) (2) Flashcards
OSA. pathophysiology? 2
Relaxation of pharyngeal muscles leads to closure of airway
Loud snoring with periods of apnea
OSA. sequelae?
Systemic hypertension
Pumonary hypertnesion and right heart failure
OSA. symptoms? 4
daytime somnolence
Non-restorative sleep with frequent awakenings
Morning headaches
Affective and cognitive symptoms
OSA. physical examination? 3
Obesity. BMI>35
Increased neck girth
Systemic HTN
OSA. what reproductive finding?
Erectile dysfunction
OSA. what findings resolves during daytime?
hypoxia and hypercapnia resolve during day unless couples with OHS.
OSA. what blood finding?
Hypoxemia –> incr. EPO –> incr. RBC and hematocrit
OSA. what method to diagnose?
nocturnal polysomnography.
OSA. nocturnal polysomnography. what diagnostic findings?
5 or more obstructive respiratory events (apnea or hypopneas) per hour is
diagnostic.
OSA. what is apnea?
Apnea: cessation of breathing for 10 or more seconds.
OSA. what is hypopnea?
Hypopnea: reduced airflow causing saturation to decrease by 4% or more.
OSA. treatment. Mild to moderate?
Mild to moderate: weight reduction, avoidance of sedatives and alcohol,
and avoidance of supine posture during sleep.
OSA. treatment. other than conservative?
Others: uvulopalatopharyngoplasty and nasal CPAP.
STOP-Bang survey for OSA. 1 point for each.
Snoring
excessive daytime Tiredness
Observed apneas or choking/gasping
high blood Pressure
BMI > 35
Age > 50
Neck size: men >17, women >16 inches
male Gender
STOP-Bang survey for OSA. points for risk?
0-2 = low risk
3-4 = intermitent risk
>= 5 –> high risk
OHS. 3 diagnostic criteria?
Obesity with BMI >=30
Awake daytime hypercapnia (PaCO2 > 45)
No alternate cause of hypoventilation
OHS. workup. ABG?
ABG on room air (hypercapnia, normal A-a gradient)
OHS. workup. x ray finding?
No intrinsic pulmonary disease on xray
OHS. workup. PFT finding?
restrictive pattern on PFTs
OHS. workup. what TSH?
normal
OHS. workup. what method diagnostic?
polysomnography
OHS. chronic hypercapnia and hypoxia on kidney?
bicarbonate retention by kidneys and decreased chloride reabsorption –> metabolic alkalosis –> blunts ventilatory response to the increased CO2 and contributes to hypoventilation.
also incr. EPO
OHS. chronic hypoxia on lung/heart?
Chronic hypoxia –> pulmonary HTN –> Cor pulmonale.
OHS. why systemic HTN occur?
Systemic hypertension due to hypoxic triggering of the SNS
and increased catecholamines.
OHS. why impaired breathing in general due to body constitution?2
Cant breathe due to excessive weight and altered lung mechanics.
OHS. what about chemoreceptors?
Wont breathe due to decreased chemosensitivity to hypercapnia due to alveolar
hypoventilation.
OHS. treatment. first line?
nocturnal positive pressure ventilation as first line
OHS. treatment. other than cpap.
Weight loss (bariatric surgery in select cases)
avoidance of sedative medication
Respiratory stimulatns (eg acetazolamide) is the last resort
OHS. treatment. respiratory stimulants?
acetazolamide
Central sleep apnea. definition?
no urge to breathe
Central sleep apnea. causes? 4
opioids
idiopathic
stroke
oxygen to COPD
Central sleep apnea. treatment - BIPAP.
.
OSA. risk factors. 4
Obesity (most common)
Tonsillar hypertrophy
Excessive soft tissue
Short mandible
OSA can also be present in combination with OHS.
.
OSA. differentials. 2
LHF and OHS.
OSA. differentials. LFH? 3
Patient might wake up in the middle of night in LHF too (paroxysmal nocturnal dyspnea)
However, patient will have difficulty every time when he goes to sleep due to orthopnea
Also, JVP is raised
OSA. differentials. OHS?
Hypoxia and hypercapnia persist throughout the day (in contrast to OSA in which there is transient hypoxia and hypercapnia only when the patient sleeps)
Patient can commonly develop pulmonary hypertension (in OSA, systemic HTN develops more commonly than pulmonary hypertension)
OHS. 5 findings?
Dyspnea, polycytemia, resp. acidosis with compensatory metabolic alkalosis, pulmonary hypertension, cor pulmonale
Note: In short, patients with OHS “can’t breathe” (due to excess weight and altered lung mechanics) and “won’t breathe” (due to decreased chemosensitivity to hypercapnia from persistent nocturnal hypoventilation)
.
M. OSA. 2 types
Can be obstructive (i.e., usually from obesity) or central (i.e., brainrelated).
M. OSA. usmles wants to know.
what disturbance, arrows CO2, bicarb, pH?
Chronic respiratory acidosis
incr. CO2, incr. bicarb, pH norma/decr..
M. OSA. what heart pathology can occur? why?
Cor pulmonale can occur as a result of pulmonary hypertension from hypoxic vasoconstriction.
M. OSA. cor pulmonale CP?
JVD or peripheral edema will be seen with cor pulmonale.
Descriptors such as RBBB, right-axis deviation on ECG, and wide splitting of S2 all mean RVH. If the patient merely has pulmonary hypertension but not yet cor pulmonale, the vignette can say loud P2 or
tricuspid regurg (holosystolic murmur that with inspiration).
M. OSA. why dysthymia/depression? was Q on tests.
Chronic fatigue and poor oxygenation can lead to dysthymia / depression.
The answer on NBME is “mood disorder due to a medical condition.”
M. OSA. Dx test?
Polysomnography (sleep study) is what USMLE wants to diagnose
M. OSA. 4 thing to know for usmle?
Disturbance/arrows
leads to pulm. hypertension -> COR PULMONALE
Can induce mental changes/depression due to poor oxygenation
Polysomnography is to establish Dx.
