Central Sleep Apnea Flashcards

1
Q

What is the primary mechanism of periodic breathing at high-altitude

A

The stimulatory effects of hypoxia opposed by the inhibitory action of hypocapnic alkalosis. Hypercapnic alkalosis induces apnea, which in turn lessens alkalotic Inhibition and augments hypoxic stimulation.This leads to poor sleep with arousals commonly occurring at the transition from the end of apnea to the onset of hyperpnea

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2
Q

What is the effective ascent to high altitude

A

Most subjects experience periodic breathing. There is a significant decrease in stage N3 slow wave sleep with an increased number of arousal is. The duration of sleep is not reduce compared to sea level
There are many arousals at the termination of apnea’s And the transition to hyperpnea

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3
Q

What is the effect of acetazolamide

A

It produces marked reduction in periodic breathing in sleep with higher and less Oscillatory SAO2. Your markedly improved both the main level and stability of arterial oxygenation during sleep and reduce the proportion of sleep time during which the periodic breathing occurred. It acts on the kidney to produce a metabolic ask a doses which drives ventilation without any clear effect on prayer for our central chemo receptor Sensitivity

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4
Q

What is the effect of low dose

Benzodiazepine

A

Shortened wake to sleep onset, decreased arousals
increased sleep efficiency, increased rem sleep
subjectively better sleep.
They augment slow wave sleep, and reduce wakefulness during acclimatization

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5
Q

What is the effect of the Theophylline at high altitudes

A

You reduce the symptoms of mountain sicknesses and improve sleep with reductions in sleep disordered breathing, the saturation, and arousals. It also causes palpitations

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6
Q

What is the initial treatment for CSAS related to CHF

A

CPAP therapy targeted to normalize the apnea hypopnea index (AHI) is indicated for the initial treatment of CSAS related to CHF. I

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7
Q

What is the role of BPAP in Spontaneous timed mode for CSAS related to CHF

A

BPAP therapy in a spontaneous timed (ST) mode targeted to normalize the apnea hypopnea index (AHI) may be considered for the treatment of CSAS related to CHF only if there is no response to adequate trials of CPAP, ASV, and oxygen therapies.

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8
Q

What is the role of nocturnal; oxygen therpay for the tretment of CSAS related to CHF

A

Nocturnal oxygen therapy is indicated for the treatment of CSAS related to CHF.

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9
Q

When is ADAPTIVE servo-ventilation useful in CHF?

A

Adaptive servo-ventilation (ASV) targeted to normalize the apnea-hypopnea index (AHI) can be used for the treatment of CSAS related to CHF in adults with an ejection fraction > 45% or mild CHF related CSAS.

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10
Q

When is acetazolamide and theophylline useful in CSAS in CHF.

A

after optimization of standard medical therapy, if

PAP therapy is not tolerated, and if accompanied by close clinical follow-up: acetazolamide and theophylline.

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11
Q

When should adaptive servo-ventilation be avoided

A

Adaptive servo-ventilation (ASV) targeted to normalize the apnea hypopnea index (AHI) should not be used for the treatment of CSAS related to CHF in adults with an ejection fraction ≤ 45% and moderate or severe CSA predominant, sleep-disordered breathing.

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12
Q

What is the treatment of CSAS in end stage renal disease

A

The following possible treatment options for CSAS related to end stage renal disease may be considered: CPAP, supplemental oxygen, bicarbonate buffer use during dialysis, and nocturnal dialysis.

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13
Q

Can zolpidem and triazolam considered for the treatment of primary CSAS

A

The use of zolpidem and triazolam may be considered for the treatment of primary CSAS only if the patient does not have underlying risk factors for respiratory depression. It is a last option

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14
Q

What is the role of Acetazolamide in primary CSAS

A

Acetazolamide has limited supporting evidence but may be considered for the treatment of primary CSAS.
Given the low overall quality of evidence and the potential for side effects including paresthesias,
tinnitus, gastrointestinal symptoms, metabolic
acidosis, electrolyte imbalance, and drowsiness, the use of acetazolamide

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15
Q

What is the effect of CPAP on LVEF

A

The random-effects meta-analysis showed that CPAP increased LVEF by 6% on average when compared with the control group.

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16
Q

Does CPAP in CSAS with CHF improve survival

A

n summary, the available data suggests that PAP may improve survival if titrated to achieve a therapeutic reduction of AHI. Conversely, PAP therapy has no effect on survival if not adequately treated. There is a decrease of 30/h [95% CI: 23 to 37] with treatment compared to baseline. Notably, residual disease, with a mean AHI of 15 ± 4, remained despite CPAP treatment

17
Q

What is risk of BIPAP in CSAS due to CHF

A

BPAP in the spontaneous mode may aggravate central apnea caused by hyperventilation.

18
Q

what is the epidemiology of central sleep apnea

A

Predominant central apnea is uncommon and is seen in less than 10% of patients presenting for PSG. In the general population, the prevalence of central sleep apnea is less than 1%. [12] CSB-CSA has been reported in 25-40% of patients with heart failure and in 10% of patients who have had a stroke. One study [6] has reported the prevalence rate of central sleep apnea at 30% in a population of patients in a stable methadone maintenance program.

19
Q

What arrhythmia occurs with CSA?

A

central sleep apnea was strongly associated with atrial fibrillation/flutter. The odds of atrial fibrillation (P = .01) and of complex ventricular ectopy (P< .001) increased with increasing quartiles of the respiratory disturbance index (a major index including all apneas and hypopneas).

20
Q

Describe High Altitude sleep CSA

A

For the diagnosis of high-altitude periodic breathing, a central apnea-hypopnea index (AHI) of greater than 5 is required at a high altitude. The usual cycle length is from 12-34 seconds. This condition also gives rise to fragmented sleep, increased stage 1 and 2 sleep, and decreased delta sleep.
It is only seen during non–rapid eye movement (NREM) sleep and improves over the course of a few days.

21
Q

Describe CSB-CSA

A

The CSB-CSA cycle in heart failure is usually triggered by an arousal resulting in large tidal volume and the consequent lowering of PaCO2.
As the patient falls asleep, the apneic threshold is elevated, and ventilation tends to oscillate around the apneic threshold, propagated by slow circulation time.
The cycle length of apnea-hyperpnea is usually greater than 40 seconds, is directly
proportional to circulation time, and is inversely proportional to cardiac output.
The arousals typically occur at the peak of the hyperpneic phase.
Criteria require the presence of at least 10 central events per hour of sleep in the crescendo-decrescendo pattern to diagnose CSB.

22
Q

What are the results of the CANPAP study

A

Canadian Prospective Continuous Positive Airway Pressure (CANPAP) trial for congestive heart failure trial. While this latter study failed to confirm a mortality benefit,

CPAP was associated with attenuation of central sleep apnea
improvement of nocturnal oxygenation
lowering of norepinephrine levels
improvement in ejection fraction
the increased distance walked in six minutes.

23
Q

What is the role of oxygen therapy in CSA

A

Oxygen is effective against high-altitude periodic breathing and improves the sleep architecture. Any patient with central sleep apnea and significant hypoxemia is a potential candidate for a trial with supplemental oxygen. The optimal flow rate can be titrated during PSG until central sleep apnea resolves.

24
Q

what is the mechanisnm for CSA syndromes

A

Sleep is characterized by elevation of arterial carbon dioxide tension (PaCO2) and a higher PaCO2 apneic threshold, the PaCO2 below which apnea occurs. Reduction of PaCO2 just a few mm Hg below the PaCO2 set point can result in apneas. Central apneic events commonly occur during the transition between wake and sleep, a period during which the PaCO2 set point adjusts.

Two types of pathophysiologic phenomena can cause central sleep apnea syndromes: 1) ventilatory instability or 2) depression of the brainstem respiratory centers or chemoreceptors.

25
Q

What are the criteria for central sleep apnea with Cheyne stokes

A

The presence of sleepiness, insomnia, frequent awakenings, or non-restorative sleep, waking short of breath, snoring, or witnessed apneas.

The presence of atrial fibrillation or flutter, congestive heart failure, or neurologic disorder.

PSG shows 5 central apnea’s/hour of sleep
Total of Central apnea’s or hypopneas is greater than 50% of the total of apnea’s and hypopneas.

Pattern of ventilation meets the criteria for CSB

26
Q

In what sleep stage does the CSB pattern tend to occur

A

During the transition from wake to N1and N2 sleep.It is less prominent in N3 and REM sleep