Weathering the Storm: COVID-19 and Mental Health, "Aftermath"
The most common and also the most insidious and potentially dangerous feature of COVID-19 is the way it compromises the lungs' capacity to oxygenate the bloodstream (hypoxemia) without us being aware of that happening. All of our organs quickly become less efficient when they do not have enough oxygen to generate energy from glucose (hypoxia). SARS-CoV-2 attacks lung tissue, including both the blood vessels and the microscopic oxygen-absorbing sacs that line the inner surface of our lungs.
In addition to damaging the blood flow in the capillaries of our lungs, the virus also damages the alveoli. Aside from triggering an immune reaction, which fills the alveoli with pus (pneumonia), the virus also affects the alveoli's production of an important protein called pulmonary surfactant. Surfactants are complex protein-lipid molecules that decrease surface tension, which is the intermolecular tension that creates a border between two compounds, in this case, blood and air. When O2-rich air enters the alveoli, it is brought into contact with O2-depleted blood coming into the lungs from the arterial blood flow and then into the lungs' arterial capillaries. Cells in the alveoli produce surfactant to allow rapid exchange of gases (perfusion) when blood in the capillaries comes into contact with air: CO2 out, O2 in. Without surfactant, the blood continues to circulate in the respiratory system, but with a much-reduced level of O2, i.e. hypoperfusion.
Pneumonia further impedes the ability of the alveoli to accomplish their perfusion task. With some forms of pneumonia, the lungs' network of capillaries can sense when there is hypoperfusion in some regions, and the blood flow will be distributed to less affected regions, maximizing the efficiency of the functioning alveolar surface area. With the SARS-CoV-2, however, because of the vascular effects on the capillary network, this response does not occur, and the lungs become even less efficient than we might expect based on other symptoms.
The cells of our vital organs have a hybrid fuel supply that allows them to continue to function with limited access to oxygen. When this occurs, cells can switch from aerobic energy to anaerobic. However, there are drawbacks to using this booster, mainly the accumulation of lactic acid. That metabolic byproduct, unlike CO2, is not just exhaled but needs to be cleared by circulating in the bloodstream to the liver and kidneys where it is broken down. As long as the heart is beating well and blood is circulating vigorously, we can briefly run short of oxygen and our cells will maintain their energy needs by switching to the anaerobic system. When the lungs are not adequately oxygenating the blood for longer periods of time, however, lactic acid can accumulate. This is especially problematic when the heart muscles are required to go without oxygen since its functioning will quickly decline, and both acute and chronic injury to the heart muscles then becomes part of a vicious cycle or cascade effect.
The result of not having enough oxygen in our blood quickly compromises how well all of our cells are functioning, especially nerve cells. Neurons in the CNS are particularly vulnerable to hypoxia for three reasons:
They don't produce their own energy but rely on “nurse cells” (glia) to support their energy needs and release metabolic byproducts under both aerobic and anaerobic conditions.
Their survival depends on staying active, requiring a constant movement of charged ions in and out of their cell membranes that constantly chat with other neurons by manufacturing, releasing and receiving neurotransmitters.
Neurons in the CNS are unique: they are the only cells in the body that don't replicate. The neurons we are born with are the ones that serve us all our lives and they die with us. CNS neurons are high-energy prima donnas: without constant attention and care from their glial cell entourage, they collapse.
Hypoxia tends to result in neurological effects in areas of the brain that have the highest need for energy: the cerebellum and the prefrontal cortex. Hypoxic injuries are most likely to result in predictable deficits of cerebellar functions, such as balance, gait, motor planning, and ocular-motor coordination. The prefrontal cortex is responsible for executive functions, which are the cognitive processes that give us the highest level of control over our behavior: flexibility, impulse control, reasoning, problem-solving, self-monitoring, sustained attention and task persistence.
What hypoxia looks like is familiar to anyone who has had altitude sickness, carbon monoxide poisoning or certain types of cardiac insufficiency: headache, dizziness, weakness, motor coordination problems, nausea, chest pain and confusion. Basically, a person with hypoxia acts like a person at the tail end of a long night of drinking. But unlike alcohol-induced confusion, irritability and clumsiness, COVID-19 hypoxia will persist as long as the lungs are not operating efficiently, and if the person is not given supplemental O2, the neurological symptoms may progress to loss of consciousness, seizures and death.
Since a COVID-19 patient may not be fully aware of the extent of their hypoxia, reliance on direct measures of oxygen saturation has become key to determining when and how to address symptoms with supplementary oxygen and/or ventilation. This is complicated by the fact that individuals may also be experiencing an altered mental status. Few invisible conditions can render a person more helpless than hypoxia.
I vividly recall getting hypoxemia from climbing at altitude in British Columbia. We were on our second day of ascending, and I had been taking aspirin periodically to try to keep altitude sickness at bay. I was struggling to keep walking steadily when my group decided to make camp. I couldn't focus my eyes or get my hands to work to set up my tent, and I really wanted to just lie down in the snow. I couldn't remember where I put the aspirin in my pack, and I couldn't get my sleeping bag open, never mind messing with my little stove to melt water or cook food. I had a splitting headache; I couldn't keep my eyes open; I felt seasick, and I wanted to be left alone. If I hadn't had some tolerant friends with me, I would have been in a dire situation.
Luckily for me, hypoxemia from being at altitude is a reversible condition. After a rest when my muscles had discharged their load of lactic acid, I was good to go. The emerging data on the longer-term effects of COVID-19 on survivors is that some will have a long road ahead of them. The rehabilitation process for many COVID-19 survivors will involve numerous hurdles, including deconditioning, resulting in a need to strengthen skeletal and respiratory muscles weakened by inactivity. We also know survivors' lung tissues may take months to fully recover from the viral damage to alveoli and capillaries, resulting in prolonged hypoxemia and periodic respiratory crises. They may need considerable monitoring for changes in alertness and other neurological signs, such as dizziness and motor coordination difficulties that can affect walking, driving and working. Anxiety, depressed mood, panic anxiety and somatic preoccupations are common in individuals with chronic illnesses, and this is likely to be the case with COVID-19 as well.
Many of us are familiar with helping individuals with chronic cardiopulmonary illnesses. They often benefit from learning to check their own blood oxygenation level using a pulse oximeter. In moments of crisis when a pulse oximeter or other O2 saturation measure has not been available, I have resorted to speaking in a slow, calm voice to patients in respiratory distress and asking to see their hand. I then press on a fingertip so they can see the change in color, which is the blood rushing back in. I then explain that if they can slow their breathing, the oxygen will get into their blood faster. I count out loud for them, emphasizing slow breathing in for about three or four seconds and then slow breathing out for five or six seconds. Air reaches into the bottom of their lungs as their diaphragm expands down, and they put their shoulders back and let their rib cage expand with each breath.
I might also ease the tension by being casual and joking, asking them about themselves or their families. Laughing dispels anxiety and stimulates the respiratory pump. I have been known to be uncharacteristically chatty and wander off-topic, distracted by the patient's photos or the books in their room. Anything to take their attention away from their labored breathing. Then I might get them to imagine a favorite place, like a holiday spot, a place at home where they relax or a familiar place to walk with their dog. The imagery helps reduce the recurrent images stirred up by dread or fears of death. Soon, the color of their fingertips brightens, and they become calmer and breathe more comfortably.
Therapists who use imagery and relaxation techniques, including meditation, may notice that I didn't get the patient to focus on their breathing. Focusing on breathing can work as a relaxation or meditation technique for physically healthy clients, but for many clients' experiencing respiratory distress, this technique can backfire. Some patients' hypoxemia will elicit gasping, but because of poor perfusion and ischemia, their diaphragm and intercostal muscles may fatigue quickly.
One of the key features of efficient breathing is the relaxation of the skeletal muscles to decrease the resistance to expansion and contraction. Therapists familiar with progressive muscle relaxation (PMR) will be familiar with the use of a series of muscle tensing followed by relaxing or loosening, which is a good distraction technique and decreases overall muscle tone, which significantly reduces basal metabolic rate (and oxygen use). The other reason for relaxation, aside from decreasing oxygen use, is for decreasing the effects of ANS sympathetic arousal effects on the brain. The last thing a person suffering from hypoxia needs is a further restriction of executive functioning caused by fight-or-flight reactions.
The cognitive and behavioral effects of anxiety are very predictable: increased mental rigidity, repetitiveness, decreased flexibility and problem-solving, exaggerated emotional responses, negativity or catastrophizing and decreased perspective-taking. It's a condition I call “wearing the microscope.” Highly anxious individuals tend to focus excessively on events they're anxious about, to magnify them, and they have difficulty seeing any other information or viewpoints. But this reaction doesn't have to be the result of just anxiety; any autonomic arousal will do: anger, lust, anticipation. They all increase the excessive focus, magnification and rigidity of behavior.
Although most of us are familiar with coping with anxiety, it can be much more complex doing so in the context of recovery from a life-threatening respiratory illness. For mental health providers, here are some important areas to keep in mind when helping those who are recovering from this very complex illness.
Check mental status frequently, but don't be annoying. Be subtle or make a joke out of it, but don't assume they're going to be clear at all times.
Know the signs and the risks of altered mental status: falling, motor vehicle accidents, impaired judgment, motor coordination difficulties, social isolation.
Few COVID-19 survivors will have been adequately screened for neurocognitive sequelae. As we know, the one organ most susceptible to the effects of hypoxia is the brain. If a COVID-19 survivor has a history of severe respiratory illness (ARDS with mechanical ventilation, or ECMO) and memory complaints, difficulties with concentration, task persistence and problem-solving persist after respiratory symptoms have resolved, request a neurocognitive screening evaluation.
Make sure clients have the means to evaluate their oxygenation levels. If a pulse oximeter is not available, check a fingertip for pinkness. Use this as a biofeedback marker.
If oxygen levels are below 90%, start by slowing down – slow your own voice, use a low tone and be casual. Don't jump right into talking about deep breathing. Make sure their heart rate is slow (below 100), and teach them to take their own pulse (unless you're already using a pulse oximeter, which will tell you their pulse).
Talk about efficient breathing. What we have learned from the successful use of ventilators with COVID-19 patients can inform how we offer breathing tips:
slower inhalation is less likely to result in stretching injuries to the lung tissue;
quick exhalation releases more CO2 and allows for spending more of the respiratory cycle on inhalation: slow in, quick out;
both inhaling and exhaling is easier when the muscles are relaxed and there is a decreased risk of fatigue;
use both intercostal and abdominal muscles to share the effort of breathing with the diaphragm. This is different from diaphragmatic breathing, which emphasizes “belly breathing,” but makes the respiratory system more susceptible to fatigue.
Teach relaxation techniques, especially involving both progressive muscle relaxation and mental imagery/distraction and meditation. This can have benefits for both compliance with beneficial breathing techniques and for improving cognition and coping.
Don't start by focusing on breathing if the patient is anxious about their breathing. You can come back to breathing after a respiratory crisis is averted by using distraction or imagery.
Screen for PTSD, especially in clients who have been hospitalized or have had close contact with others with life-threatening symptoms. Don't assume that clients who have been in rehabilitation have already been asked about PTSD symptoms.
Don't be afraid to use humor. Laughing is a great exercise for anxiety and breathing.
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