Heart Failure and Sleep Apnoea

A Lecture on the Interaction between Heart Failure and Sleep Apnoea

by Matt Naughton

A Background on Heart Failure

During Heart Failure, the heart starts to dilate and is unable to pump blood adequately to maintain all the bodily organs. The commonest symptom is breathlessness on exertion, and often patients will be breathless at rest. It affects somewhere between one and two percent of the population, making it a common disorder, and that prevalence is increasing, having doubled over the past 25 years. This increase is thought to be related to the improved survival rate people now have after heart attacks, due to MICA, modern treatment techniques, etc. Consequently, there is now an increased number of people with damage to their heart muscles as a result of those heart attacks.

Heart failure is associated with clots to the lung, stroke, and also large vessel disease. People who have heart disease have a mortality rate at the five year mark of around 50%, which is on par with a number of malignancies (cancers and tumours), making it an important disease to recognise and treat.

Notably there has not been a great increase in the survival rate between 1948 and 1988. Slide, 1993 data: comparing data till 1974 and data till 1993, over an 8 year period, the survival of neither males nor females with heart disease has improved.

This indicates that perhaps we should be looking for new risk factors; smoking, hypertension, and cholesterol are the established risk factors, but what we are missing is additional risk factors, the understanding of which might help improve the survival from heart disease, and that is where we think that Sleep Apnoea may be relevant.

Sleep Apnoea and Heart Failure

The pertinent question: "How prevalent is apnoea in people with heart failure?" We are talking about people with Congestive Heart Failure - impairment or damage to the left ventricle.

Three research papers have addressed this:

The first study (done at The Alfred Hospital), looked at 75 heart patients, mostly male. The bottom line was that the number of people with either central or obstructive apnoeas is about 60%. Comparable and corroborative results were achieved here. One can see that the prevalence of those with apnoea amongst those with established heart failure is around two thirds.

The results are influenced by the study group - roughly speaking, are they Clinic or Heart Transplant? The proportion of these patients showing central sleep apnoea (as apposed to obstructive apnoea) is roughly 50/50, though this varies.

Progress of Heart Function

With no apnoea there are these various phases:

Applied medications include captopril, enalapril, more recently beta blockers and others are able to improve heart function. Life-style factors such as smoking, alcohol consumption, weight and exercise are also effective.

Up to this point patients are relatively normal, or may have impaired function but are quite static, or improve and decline but are essentially maintaining satisfactory heart function compared with descent into severe heart failure

In addition there may be reduced life expectancy amongst those with heart conditions in relation to other causes of premature death compared to the normal population.

With sleep apnoea, patients have more ups and downs oscillating in the precariousness of their condition.

These phases manifest:

Some patients oscillate from one group to the other during their time in heart failure.

We do not know what proportion of people with obstructive sleep apnoea go on to develop heart failure, but it is probably a risk factor, as is, for example, smoking (approximately 10 to 15% of smokers develop heart disease. The rest do not.)

Where you have a person who has high cholesterol, and is diabetic, overweight or does insufficient exercise, their chances of developing heart disease are greater. Of course, they may still never develop the heart disease. However, when patients do develop heart failure, we believe that they will then go on to develop central sleep apnoea.

Obstructive Sleep Apnoea

Obstructive apnoea is often associated with snoring, though some women do not snore, yet still they have apnoeas. They may present with EDS, paradisaical nocturnal dyspnoea (breathless at night), orthopnea (breathlessness lying flat), nocturnal angina.

The connection to obstructive sleep apnoea is probably related to Hypertension. There is now very good evidence that obstructive apnoea (untreated) contributes to high blood pressure, which is a risk factor for heart failure, and this may be one of the links that connects the two. Another is that people with obstructive sleep apnoea have a greater chance of heart attack, myocardial infarction, and that, independent of blood pressure, can contribute to the onset of heart failure.

Extra Risk Factors

If you have obstructive sleep apnoea or central sleep apnoea does that effect the prognosis of the diagnosis?

The primary symptomatic distinction of central sleep apnoea from obstructive sleep apnoea is that with central sleep apnoea you get the orthopnea (breathlessness lying flat in bed), and paradisaical nocturnal dyspnea (waking up at night short of breath.) Note that there may be other reasons for both of these symptoms eg asthma, heartburn, obstructive sleep apnoea too. However, if someone is regularly waking up short of breath, central sleep apnoea should be considered. They have fragmented and restless sleep sometime due to fear of sleep, due to great stress.

Note first that obstructive sleep apnoea patients hypoventilate and central sleep apnoea patients hyperventilate. Recent work has involved understanding the mechanisms that cause this.

  1. Lung Pressure
    Water in the lungs (which occurs when people have heart failure) can be sensed by very small nerves which connect to the vagus nerve, which travels up through the centre of the body to the brain. On measuring lung pressure (specifically, the pressure inside the blood vessels within the lung) for breathing effects, it is found that the central sleep apnoea group has a much higher pressure as compared to obstructive sleep apnoea or non-apnoea groups of patients, but that there is significant overlap between the three groups. Therefore the pressure in the lungs can only be indicative of central sleep apnoea, but cannot be the sole mechanism or causative factor.
    Further to this, and noting that lung transplant patients (there is a convenient lung transplant unit actually at the Alfred) have had this nerve deliberately cut, another piece of data was telling. One of these lung transplant patients developed signs of both heart failure and central sleep apnoea but, since he had no vagus nerve connection, was an important exclusive case (has the condition, doesn't have the nerve). Based on his counter example, it is likely that this mechanism (i.e. the vagus nerve connection) has only a small role in central sleep apnoea.
    Note that this is not the case for animals, such as dogs, which are far more vagal animals, so amongst which vagal input is much stronger.
  2. The blood gas, or the circulations side, involving the level of O2, CO2 and pH or Acidity of the blood. These are sensed by two thermistors (like thermostats) - quick peripheral chemo-receptors located in the neck. Peter Solan, now at Monash Medical Centre, and who completed his PhD with me, did a study relating CO2 levels in the blood to heart failure and apnoea patients.
    From this study, it is very clear that those with central sleep apnoea have a more sensitive response to variation of CO2 levels than obstructive sleep apnoea or non-apnoea heart patients. A slight fluctuation in the level of CO2, and the brain over shoots, or overreacts, in its level of response. It is also evident that the obstructive sleep apnoea group tends to be less severe in terms of heart failure than the central sleep apnoea group. This is consistent with earlier remarks in this lecture regarding the tendency of severe heart failure to correlate with central sleep apnoea.

Other studies have confirmed this result. For example, a study in Japan, utilising rabbits. Creating heart failure in the rabbits, the researchers biopsied the equivalent thermistors in the rabbits, and found that the histology and anatomy of these thermistors was changed by the onset of heart failure, and that this change manifested in a particular sensitivity and over response to small fluctuations of CO2 in the blood. This was consistent with Peter Solan's results.

Having established that for patients with both heart failure and central sleep apnoea the problem is incorrect function of these thermistors, the salient question is: why? The short answer: We are unsure.

One of our suspicions reflects a feature of heart failure, that the stress hormones go very high, of a similar degree to those experienced by the victim of an armed mugging at an auto-teller. One of the things that we is that when stress hormones are activated, the sensitivity of these thermistors in our necks increases. There is a strong relationship between the amount of catecholamines and stress hormones(as measured in blood, urine and the heart itself) released into the blood. Which ever way we look at it, the amount of stress hormone is elevated in patients with central sleep apnoea. It appears to correlate very closely with the severity of the central sleep apnoea, and also with the severity of hyperventilation.

Both thermistors are increased in their activity. We have a very quick acting peripheral thermistor, and a slower acting central one. One correlates with background ventilation during wakefulness, the other with the speed at which we can turn on and off our breathing pattern during central sleep apnoea.

What is the relevance of this information?


The primary therapy is still pharmacological, and drug dosages are commonly increased.

Oxygen is used but its been found that it's not that effective for central sleep apnoea and sometimes detrimental.

Sedatives re hyperventilation - no benefit.

Additional co2 - rapid breathing all the time, no good. It turns off the central sleep apnoea, but the patients breath rapidly all the time.

CPAP machines (continuous positive airway pressure)

CPAP Machines

(The use of) CPAP machines to improve cardiac function, to reduce the amount of ventilation required, reduce the stress hormone sympathetic activity, and to improve the strength of the respiratory muscle (by allowing resting of the inspiratory muscles) over a three month period. Reduces stress, heart upstream pressure, reduces the size of the heart (small compact hearts are better than large hearts), reduces the amount of cardiac work, so that the heart is more efficient, we believe it makes the respiratory muscles work more efficiently, increases the volume of air in the lungs (50% of the bodies oxygen stores is in the lungs), and therefore the amount of oxygen available to the body. Heart failure victims have small lungs because their hearts have generally dilated due to the heart failure, and fluid builds up at the bases of the lungs, and the muscles are often weak (called a restrictive ventricle defect). By maintaining positive pressure we open up the chest, preventing fluid getting into the little alveoli sacks, preventing fluid accumulating in the lung bases, and we are assisting the respiratory muscles. In total, this increases the lung volume.

If CPAP does not work, there is a new machine which could be characterised as a respiratory pattern pace maker. In a patient who has periods of no breathing, this machine kicks in and initiates breathing. It is a new machine, but it is early days, and there is much to be known about the effect on parameters relevant to heart failure patients.

The state of play now is that we are focusing on more preventative approaches and specifically at the moment, focusing on CPAP.

Further Reading

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