Lecture 13 Abnormal Breathing Patterns I PDF

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PHYL 4504/5404: Abnormal Breathing Patterns; The Respiratory System under Stress

At the end of this lecture, the student should be able to:

1. Diagram the abnormal breathing patterns seen in obstructive and central sleep apnea, Cheynes- Stokes, Biot’s and Kussmaul’s respiration and recognize their causes 2. Be able to explain the relationship between altitude and barometric pressure and how this affects alveolar and arterial gases 3. List the acute effects of hypoxia 4. Know the symptoms of acute and chronic mountains sickness 5. Be able to explain the 5 main mechanisms of acclimatization to high altitude

By the end of this lecture, you should be able to answer the following questions. 1. Which is most common- obstructive or central sleep apnea?  Obstructive 2. Which type of abnormal breathing pattern is a type of hyperventilation?  Kussmaul respiration 3. What is the approx. PO2 at the summit of Mount Everest?  43 mmHg 4. An increase in hemoglobin concentration in the blood (and therefore an increase in oxygen-binding capacity) is called what?  polycythemia 5. Is the hypoxic pulmonary vasoconstriction seen as an adaptation to altitude generally more beneficial or harmful? – Harmful

Remember to input your answers on Brightspace in the section: Quick Quiz: Abnormal Breathing Patterns; Respiratory System under stress (Oct 19) before midnight on Oct 25th. This material will be tested in the unit quiz on October 26th

Sleep Apnea- Obstructive 1.

Obstructive Sleep Apnea (OSA) Apnea = the absence of spontaneous breathing Apnea results in significant decreases in PO2 and increases in PCO2 Most common type Occurs when the upper airway – usually the hypopharynx (bottom part) - closes during inspiration Airway totally obstructed and airflow stops Hypercapnia and hypoxemia occur depending on length of it Episodes can last 10 seconds or longer, 300-500 times each night, can be quite disruptive to sleep

Pleural pressure oscillations increase as CO2 rises.

Increased CO2 stimulates respiratory urge = sudden attempt to breathe, loud snorts, gasps, snoring Resistance to airflow is very high as a result of the upper airway obstruction

Berne and Levy, Fig 24-8A

Obstructive Sleep Apnea Risk factors: age, gender (male), obesity, increased neck circumference, Use of alcohol or sedatives, certain craniofacial abnormalities. Weight gain: 10% increase in weight = 32% increase in # of apneas Symptoms: • Excessive daytime sleepiness/ sleeping at inappropriate times • Unrefreshing and/or restless sleep • Morning dry mouth • Morning headache • Difficulty concentrating • Irritability, mood changes • Snoring • Nocturnal choking

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Nocturnal cardiac arrhythmia Erythrocythemia

Treatment: CPAP(continuous positive air pressure) - dilates the upper airway, preventing closure Dental Appliances- mandibular advancement splints Surgery- soft palate alterations

Sleep Apnea - Central Characterized by breathing that stops and starts during sleep. Occurs when the CNS drive to the ventilatory muscles is transiently abolished Distinguished from obstructive sleep apnea by a lack of respiratory effort. Causes include damage to the central respiratory areas or abnormalities of the neuromuscular apparatus or are unknown. High altitude can induce this. Patients are extremely sensitive to small doses of sedatives or narcotics, which further reduce the responsiveness of the respiratory centres to the stimulatory effects of CO2 Repeated episodes of apnea, during which patient makes no respiratory effort. Degree of hypercapnia and hypoxemia less than in OSA

No attempt to breath is made as demonstrated by lack of oscillations in pleural pressure Only about 1% of sleep apneas are pure “central” although about 10% may represent a mixed obstructive/central pattern Berne and Levy, Fig 24-8B

Breathing Patterns

Normal

Effect of removing sensory input from lung receptors (mainly stretch) Each breathing cycle is lengthened, and tidal volume increased so alveolar ventilation is not affected

Apneustic breathing Input from cerebral cortex and thalamus eliminated with vagal blockade Loss of inspiratory-inhibitory activities resulting in loss of inspiratory drive Result is prolonged inspiratory activity broken after several seconds by brief expirations (apneusis). Seen in patients with CNS damage (stroke, trauma)

Berne and Levy, Fig 24-10

Cheyne’s-Stokes Breathing

Abnormality of ventilatory control Characterised by varying tidal volume and ventilatory frequency After a period of apnea, VT and respiratory frequency increase over several breaths- then decrease until apnea occurs again Periods of apnea can be 10-20 seconds Oscillatory changes in blood-gases occur Often a sign of low cardiac output Also seen at high altitude. Brain injury. Proposed Mechanism: Increased ventilation leads to decreased CO2 and increased O2. It takes seconds before this changed blood composition reaches the central chemoreceptors to inhibit the excess ventilation. By this time, the person has already overventilated for a few seconds- when this “overventilated” blood reaches the brain respiratory centre, the centre becomes over-depressed- and the opposite cycle begins (decreased ventilation, CO2 increases and O2 falls). Again, takes time for brain can respond…when it does, the cycle starts again Berne and Levy, Fig 24-9

Biot’s and Kussmaul’s Respiration

Biot’s respiration: abnormal pattern of breathing characterized by groups of quick, shallow inspirations followed by regular or irregular periods of apnea. Often difficult to distinguish from Cheynes-Stokes Caused by damage to the pons (strokes, trauma) or pressure on the pons due to herniation. Opioid use

Kussmaul’s respiration: deep and labored breathing pattern (hyperventilation) often associated with severe metabolic acidosis, especially diabetic ketoacidosis. Respiratory compensation for metabolic acidosis

https://www.youtube.com/watch?v=ViGjOiPE2mY

High Altitude

Relationship between altitude and barometric pressure

Barometric pressure decreases with distance above the earth’s surface Pressure at 19,000 ft is approx. is one-half sea-level value of 760 mmHg PO2 of moist inspired gas = (380 – 47*) x 0.21 = 70 mmHg

West Resp Physiology Fig 9.2

At summit of Mount Everest (29,028 ft), inspired PO2 is 43 mmHg Significant hypoxia associated with high altitude…however, many people live permanently at altitudes higher than 16000ft and climbers have ascended Everest without use of supplemental oxygen. * remember 47 mmHg is partial pressure of water vapour at body temperature.

Changes in alveolar and arterial partial pressures at altitude Normal Sea Normal Altitude: Sea Level

Summit of Mount Everest: 29,028 ft above sea level Barometric P : - 228 mmHg P O2: 48mmHg

Barometric P : - 760 mmHg P O2: 160 mmHg

35 mmHg 7.5 mmgH g

Arterial pH = 7.4

P O2 = 28mmHg P CO2 = 7.5mmHg Arterial pH = 7.8

Even at high altitudes, CO2 is continually produced and transferred into alveoli and water vaporizes into inspired air from respiratory surfaces. These gases ‘dilute’ O2 in alveoli, reducing O2 concentration At altitude, alveolar PCO2 falls, especially in acclimatized persons, due to increasing ventilation (rate can be up to fivefold higher) At 20,000 ft alveolar PO2 falls to about 40 mmHg in unacclimatized vs 53 mmHg in acclimatized person because alveolar ventilation increases more in acclimatized people

Above 10,000 ft Hb-O2 saturations starts to fall Breathing pure O2, most of the space in alveoli occupied by N2 now can be filled with O2: therefore significant effects on arterial O2 saturation (red vs blue curves)

Acute Effects of Hypoxia Acute effects of hypoxia in an unacclimatized person (start at approx. 12000 ft): Drowsiness, lassitude, mental and muscle fatigue, sometimes headache, occasionally nausea, sometimes euphoria Above 18,000 ft: twitching and seizures Above 23,000 ft: coma, death Significant problem is decreased mental capacity, which decreases judgement, memory and performance of discrete motor movements. Unacclimatized person stays at 15,000 ft for one-hour, mental proficiency falls to about 50%. After 18 hours, approx. 20% of normal. Death Zone: starts at 26,000 ft . Many mountaineering deaths occur at this altitude either directly, due to loss of physiological functioning, or indirectly, due to wrong decisions made as a result of decreased mental capacity. An extended stay in the zone without supplementary oxygen will result in deterioration of bodily functions, loss of consciousness, and death

Mountain Sickness-acute and chronic Small number people who ascend quickly (no acclimatization) can become very sick quickly, can be fatal 1. Acute cerebral edema Believed to be the result of local vasodilation of the cerebral blood vessels, due to hypoxia Vasodilation increases blood flow into the capillaries, increasing capillary pressure and causing fluid to leak into the cerebral tissues. Cerebral edema can lead to severe disorientation 2. Acute pulmonary edema Cause still unclear, but genetic factors may play a role Possible hypothesis: severe hypoxia causes pulmonary arterioles to constrict, but constriction is not uniform. More and more blood in pulmonary vasculature is pumped through fewer and fewer non constricted vessels. Increasing capillary pressure in these parts of lung becomes very high, resulting in fluid leakage and local edema. Process extends throughout lungs, so pulmonary edema spreads with associated loss of function Chronic: can develop in person remaining at high altitude •Red blood cell mass and hematocrit become very high, increasing blood viscosity. This will decrease blood flow to tissues and O2 delivery will fall •Pulmonary arterial pressure becomes even more elevated as arterioles vasoconstrict due to hypoxia. Usual vasoconstrictive mechanism, but now all parts of lung have low O2 so pulmonary arterial pressure rises excessively. •Right heart becomes greatly enlarged and starts to fail •Peripheral arterial pressure falls •Congestive heart failure occurs = death if not moved to lower elevation

Acclimatization If person stays at high altitude for an extended period, they adapt to the decreased PO2 and deleterious effects of hypoxia decrease. They are then able to work harder without hypoxia, or ascend further Main mechanisms of acclimatization: 1.Hyperventilation 2.Increased number of red blood cells (polycythemia) 3.Increased vascularity in the peripheral tissues 4.Increased efficiency of cells to use O2 5. Increased diffusing capacity of the lungs

Hyperventilation Immediate exposure to low PO2 stimulates peripheral chemoreceptors to increase ventilation rate to max of 1.65 times normal. Very rapid compensation occurs within seconds and permits person to ascend several thousand feet higher than without increased ventilatory response. Several days at altitude: chemoreceptors can increase ventilation more, to 5X Immediate increase in ventilation results in more expired CO2 and increased pH (alkalosis) – result is inhibition of brain stem respiratory centre which opposes the effect of low PO2 to stimulate respiration via peripheral chemoreceptors – opposite to what you want. However, this effect fades between 2-5 days, due to renal excretion of HCO 3- and consequent decrease in pH of CSF which decreases pH in fluids around chemo-sensitive neurons in respiratory centre and increasing respiratory stimulation

Acclimatization (2)

Acclimatization (3) For people living in Peruvian Andes (15000ft), PaO2 is 45 mmHg and corresponding arterial O2-saturation is 81%. Normally, this would significantly decrease total arterial O2 but due to effects of polycythemia, Hb concentration is increased giving an arterial O2 conc of 22.4 ml/100 ml: actually higher than normal person at sea level! Polycythemia also maintains PO2 in mixed venous blood which is typically only 7mmHg less than normal Stimulus for increased red blood cell production is hypoxemia, which triggers erythropoietin production from the kidney and which stimulates increased erythrocyte production in the bone marrow. Also raises blood viscocity- not good.

PO2 values from inspired air to mixed venous Blood at sea level compared to residents at 15,000 ft (4600m). In spite of the much lower inspired PO2 at altitude, the PO2 of mixed venous blood is not too dissimilar

West Resp Physiology Fig 9.3

Acclimatization (4) Increased vascularity in the peripheral tissues Cardiac output can increase approx. 30% immediately after moving to high altitude. However, this decreases during acclimatization over next weeks as blood hematocrit increases. result is total O2 transported to periphery remains constant Also increased growth of systemic circulatory capillaries in non-respiratory tissues, angiogenesis Occurs especially in animals and people born at high altitude; less so in people moving to altitude.

In animals native to altitudes between 13-17,000 ft, cell mitochondria and oxidative enzymes are more plentiful than at sea-level. Therefore, it is assumed that cells in people who have acclimatized can use O2 more efficiently at the cellular level Hypoxia induces HIFs (hypoxia-inducing factors), DNA-binding transcription factors that induce several genes that enhance O2 delivery to tissues and enhance energy metabolism Some genes controlled by HIFs include: • Genes associated with vascular endothelial growth factor, which stimulates angiogenesis • Erythropoietin genes, which stimulate red blood cell production • Various mitochondrial genes associated with energy utilization • Glycolyic enzyme genes involved with anaerobic metabolism

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Genes that increase availability of NO, which increases pulmonary vasodilationAcclimatization (5)

• Increased Diffusing Capacity • Normal diffusing capacity for O2 through pulmonary membranes is approx 21 ml/mm Hg/min This can increase three-fold during exercise and also at high altitude • There is increased pulmonary capillary blood volume, which expands capillaries and increases surface area available for diffusion • Also increased pulmonary arterial pressure, which forces blood into more alveolar capillaries, especially in upper parts of the lung: improves VQ distribution. • Pulmonary vasoconstriction occurs in response to alveolar hypoxia, increasing pulmonary artery pressure and the work done by the right heart. This hypertension can be exaggerated by the polycythemia (increased viscosity) and can lead to hypertrophy of right heart. • May result in more uniform blood flow, though sometimes results in pulmonary edema. • • •

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Summary

• Abnormal Breathing Patterns • Central and Obstructive sleep apnea • Cheynes-Stokes, Biot’s and Kussmaul’s • Effects of High Altitude • Significant hypoxia associated with high altitude including drowsiness, lassitude, mental and muscle fatigue, headache, nausea. • Acute cerebral and pulmonary edema may occur, which can rapidly become fatal • People have the capacity to acclimatize to high altitude. However, people born as lowlanders can never achieve the same beneficial effects from acclimatization as those born at altitude. • Acclimatization to High Altitude • Most important feature is hyperventilation • Polycythemia is slow to develop and of less importance (although permits people to live at 15000ft) • Increase in cellular oxidative enzymes • Increased vascularity in the peripheral tissues • Increased diffusion capacity • Hypoxic pulmonary vasoconstriction is not beneficial...