It is important to have a plan to manage episodes when you experience shortness of breath. Your health care provider might recommend complementary therapies to manage dyspnea without medication, such as:. Sometimes, relieving shortness of breath without the use of medication may not work. There are different ways to treat shortness of breath with medication, including:. Short-acting benzodiazepines, a type of anxiety medication, to relieve anxiety caused by shortness of breath.
Shortness of Breath or Dyspnea Approved by the Cancer. Common symptoms of dyspnea include: Uncomfortable breathing Shortness of breath Not being able to get enough air A feeling of smothering, tightness, drowning, or suffocation Finding the cause of shortness of breath A person may have dyspnea even though the actual levels of oxygen are within a normal range. To learn more about your symptoms, your health care team will: Review your medical history Ask you to describe your symptoms and what makes them worse Ask you to rate your symptoms on a scale Causes of shortness of breath Dyspnea may be caused by a tumor or another condition related to cancer.
Your health care provider might recommend complementary therapies to manage dyspnea without medication, such as: Breathing techniques Relaxation techniques Distraction strategies Posture techniques Physical therapy Acupressure, which is when physical pressure is applied to acupuncture points Reflexology, which applies pressure to the feet, hands, and ears Sometimes, relieving shortness of breath without the use of medication may not work.
Coping With Cancer. Find a Cancer Doctor. An observational study by Lenglet et al 11 showed that HFNC decreased dyspnea scores compared with COT in subjects with acute respiratory failure presenting to an emergency department. Furthermore, Schwabbauer et al 12 found that HFNC significantly reduced dyspnea and improved comfort compared with noninvasive ventilation in subjects with hypoxemic respiratory failure.
In addition, the subjects in the present study tolerated HFNC very well, and no serious adverse events occurred during the study period. Furthermore, subjects who received HFNC trended toward reduced hospitalization, but this was not found to be statistically significant. Improvement of dyspnea by HFNC can be explained by several mechanisms, including the high gas flow matching subjects' demand, 13 decreased pharyngeal dead space, 5 , 14 , 15 low levels of positive airway pressure, 16 — 19 improved thoracoabdominal synchrony, 20 and reduced symptoms of mucosal dryness with heated-and-humidified gas.
The advantage of HFNC in terms of improving dyspnea, subject comfort, and oxygenation has also been noted in other subject populations, such as post-cardiac surgery 8 and post-endotracheal extubation subjects, 7 , 9 and during fiberoptic bronchoscopy.
Several studies demonstrated that HFNC reduced breathing frequency and also improved oxygenation in subjects with acute respiratory failure. This could be explained by the effect of specific treatments such as bronchodilator medications or diuretics, which had time to act and modified the pathophysiology of the subjects' presentation.
Patients receiving HFNC should be closely monitored using parameters similar to those used during noninvasive ventilation.
In addition, in a retrospective observational study on subjects with acute respiratory failure, Kang et al 35 found that HFNC failure led to delayed endotracheal intubation and worse clinical outcomes. In the present study, no subject was intubated or received noninvasive ventilation because they were less sick compared with the subjects in the abovementioned studies.
Thus, appropriate selection and frequent re-evaluation of patients during HFNC use will help to improve outcomes, particularly in the emergency department.
This study has some limitations. First, there was a 1. Second, we did not measure delivered F IO 2 in the COT group because this technique was difficult to perform in the emergency department. Third, arterial blood gases were not measured during the study. This was an important limitation for comparing gas exchange between the 2 groups and the potential changes in P aCO 2 from oxygen therapy, particularly in subjects with COPD.
In conclusion, HFNC resulted in less dyspnea and better comfort in comparison with COT in subjects presenting to the emergency department with acute dyspnea and hypoxemia. This device may benefit patients requiring oxygen therapy in the emergency department. The authors have disclosed no conflicts of interest.
See the Related Editorial on Page NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address. Skip to main content. Research Article Original Research. Nuttapol Rittayamai. Introduction Acute dyspnea with accompanying hypoxemia is a major problem in emergency departments.
QUICK LOOK Current knowledge Heated-and-humidified O 2 delivered by high-flow nasal cannula reduces ventilatory requirements by flushing the anatomic dead space and improves oxygenation by meeting inspiratory flow demands. What this paper contributes to our knowledge Heated-and-humidified high-flow O 2 resulted in less dyspnea and better comfort compared with conventional O 2 therapy COT in subjects presenting to the emergency room with acute dyspnea and hypoxemia.
Methods Subjects and Study Design A prospective randomized comparative study Thai Clinical Trials Registry identifier TCTR was conducted from May to November in an emergency department of the Faculty of Medicine Siriraj Hospital in Bangkok, Thailand, to investigate the effects of HFNC in terms of physiologic changes dyspnea, breathing frequency, oxygenation, and comfort , adverse events, and hospitalization rate compared with COT in subjects with acute dyspnea and hypoxemia. Protocol The eligible subjects were randomized into 2 groups with a blind envelope pull.
Data Collection Baseline demographic and clinical data were collected. Results Baseline Characteristics Forty subjects were enrolled in this study Fig. Flow chart. View this table: View inline View popup Download powerpoint. Table 1. Baseline Characteristics of the Groups of Randomized Subjects. Table 2. Adverse Events and Hospitalization Rate No serious adverse events occurred. Conclusions In conclusion, HFNC resulted in less dyspnea and better comfort in comparison with COT in subjects presenting to the emergency department with acute dyspnea and hypoxemia.
E-mail: nuttapol. References 1. Emergency oxygen use in adult patients: concise guidance. Clin Med ; 11 4 : — Physiologic effects of noninvasive ventilation during acute lung injury. BTS guideline for emergency oxygen use in adult patients. Thorax ; 63 Suppl 6 : vi1 — vi Ricard JD. High flow nasal oxygen in acute respiratory failure.
Minerva Anestesiol ; 78 7 : — OpenUrl PubMed. Research in high flow therapy: mechanisms of action. Respir Med ; 10 : — High-flow oxygen therapy in acute respiratory failure. Respir Care ; 55 4 : — High-flow nasal cannula versus conventional oxygen therapy after endotracheal extubation: a randomized crossover physiologic study. Respir Care ; 59 4 : — In early December , the first cases of a pneumonia of unknown origin were identified in Wuhan, the capital of Hubei province in China. Although much is known about the epidemiology and the clinical characteristics of COVID, little is known about its impact on lung pathophysiology.
Many patients present with pronounced arterial hypoxemia yet without proportional signs of respiratory distress, they not even verbalize a sense of dyspnea [ 4 , 5 , 6 , 7 , 8 ]. Tobin et al. In patients with COVID, the severity of hypoxemia is independently associated with in-hospital mortality and can be an important predictor that the patient is at risk of requiring admission to the intensive care unit ICU [ 9 , 10 ].
Since correct recognition of hypoxemia has such an impact on prognosis and timely treatment decisions, we here offer an overview of the pathophysiological abnormalities in COVID that might explain the disconnect between hypoxemia and patient sensation of dyspnea.
Breathing is centrally controlled by the respiratory center in the medulla oblongata and pons regions of the brainstem see Fig. The main input affecting the respiratory drive is derived from chemical feedback among peripheral and central chemoreceptors.
The center is, however, also influenced by higher brain cortex, hypothalamic integrative nociception, feedback from mechanostretch receptors in muscle and lung, and metabolic rate. The output of the respiratory center can be divided into rhythm- e. It should be distinguished from tachypnea rapid breathing or hyperpnea increased ventilation.
Dyspnea grading relates to whether this feeling occurs in rest or upon exercise. This semi-quantitative approach of scoring is best exemplified by the frequently used modified Medical Research Council MRC dyspnea scale, which categorizes dyspnea from grade 0 dyspnea only with strenuous exercise to grade 4 too dyspneic to leave house or breathless when dressing in relation to subjects of the same age [ 15 , 16 ].
Various sensory, pain and emotional stimuli affect the sensation of breathing via the cerebral cortex and hypothalamus [ 17 , 18 ]. The abnormal sense of muscle effort is another contributor to dyspnea.
Conscious awareness of the activation of respiratory muscles is absent in healthy breathing. However, when the respiratory muscles are fatigued or weakened due to altered lung mechanics e. Dyspnea can also be caused by input from the mechanoreceptors in the respiratory tract and the chest wall. Stimulation of vagal irritant receptors e.
The contribution of metabolic rate in modulating sense of dyspnea in critically ill patients remains unclear, despite its well-established role during exercise [ 11 , 21 ]. The best-known determinants of the respiratory drive are the central and peripheral chemoreceptors. Changes in partial gas pressure of dissolved carbon dioxide in the blood PaCO 2 seem the most important component, causing shifts in pH at the level of both the peripheral and central chemoreceptors [ 11 , 12 , 22 ].
At steady state, the arterial PaCO 2 is determined by the following equation:. The normal response to hypercapnia caused by increased V D , hypoventilation or increased VCO 2 is an increase in respiratory drive and minute volume ventilation [ 23 ].
Hypoxemia itself rather plays a limited role in the sensation of breathlessness experienced by patients with cardiopulmonary disease on the opposite of hypercapnia that creates per se dyspnea [ 12 , 24 , 25 ]. Many patients with dyspnea are not hypoxemic, while those who are, usually experience only a slight improvement in symptoms after hypoxemia is corrected with supplemental oxygen therapy [ 12 ]. Of note, the normal response to hypoxemia is a rise in minute ventilation, primarily by increasing tidal volume and respiratory rate.
Increased respiratory rate tachypnea and tidal volume hyperpnea - and not dyspnea - are therefore the most important clinical signs of impending hypoxemic respiratory failure [ 11 , 27 ]. Furthermore, PaCO 2 serves as one of the fundamental regulators of cerebral blood flow. Hyperventilation causes decreased PaCO2 which subsequently leads to arterial vasoconstriction thus lowering cerebral blood flow and intracranial pressure. In contrary, increase in PaCO 2 leads to increased intracranial pressure ultimately leading to deteriorating level of consciousness, altered brainstem reflexes, and altered postural and motor responses [ 28 , 29 ].
The disconnect between the severity of hypoxemia and the relatively mild respiratory discomfort reported by the COVID patients contrasts with the experience of physicians usually treating critically ill patients in respiratory failure [ 30 ]. Guan reported dyspnea in only Happy or silent hypoxemia is not exclusively seen in COVID, but may also occur in patients with atelectasis, intrapulmonary shunt i. Rapid clinical deterioration may occur. Oxygen saturation measured by pulse oximetry SpO 2 is often used to detect hypoxemia.
The sigmoid shaped oxyhemoglobin dissociation curve seems to shift to the left, due to induced respiratory alkalosis drop in PaCO 2 because of hypoxemia-driven tachypnea and hyperpnea. During hypocapnic periods, the affinity of hemoglobin for oxygen and thus oxygen saturation increases for a given degree of PaO 2 , explaining why SpO 2 can be well-preserved in the face of a profoundly low PaO 2 [ 33 , 34 , 35 ].
This finding is also seen in high altitude hypoxemia, in which hypocapnia significantly shifts the oxygen-hemoglobin dissociation curve and improves blood oxygen saturation [ 36 ]. The alveolar gas equation also predicts that hyperventilation and the resulting drop in the alveolar partial pressure of carbon dioxide leads to an increase in the alveolar partial pressure of oxygen and ultimately lead to an increase in SpO 2 [ 22 ].
Liu et al. This leads to the production of large amounts of serum ferritin to bind these free irons in order to reduce tissue damage [ 37 ]. In conclusion, SpO 2 should be interpreted in the light of the presence of hyperventilation tachypnea, low P a CO 2 and, if possible, P a O 2 via arterial puncture. This can be performed rapidly on a smartphone app [ 38 ].
The infection leads to a modest local interstitial edema, particularly located at the interface between lung structures with different elastic properties, where stress and strain are concentrated [ 27 ]. Due to increased lung edema leading to ground-glass opacities and consolidation on chest imaging , loss of surfactant and superimposed pressure, alveolar collapse ensues and a substantial fraction of the cardiac output is perfusing non-aerated lung tissue, resulting in intrapulmonary shunting [ 27 ].
As previously discussed, tidal volume increases during the disease course leading to rising negative inspiratory intrathoracic pressure. The latter, in combination with increased lung permeability due to inflammation, will eventually result in progressive edema, alveolar flooding, and patient self-inflicted lung injury P-SILI , as first described by Barach in [ 11 , 40 , 41 ].
Over time, the increased edema will further enhance lung weight, alveolar collapse, and dependent atelectasis, resulting in progressively increasing shunt fraction and further decline of oxygenation which cannot completely be corrected by increasing F i O 2.
The persistence of high pulmonary blood flow to non-aerated lung alveoli appears to be caused by the relative failure of the hypoxic pulmonary vasoconstriction mechanism constriction of small intrapulmonary arteries in response to alveolar hypoxia during SARS-CoV-2 infection, as recently illustrated by Lang et al.
Whether the latter mechanism is only triggered by the release of endogenous vasodilator prostaglandins, bradykinin, and cytokines associated with the inflammatory process or also by other yet undefined mechanisms remains to be investigated [ 33 , 44 , 45 ]. Vasoplegia also seems to be influential in the loss of lung perfusion regulation, possibly induced by shear stress on the interfaces between lung structures, as part of the P-SILI spectrum [ 45 , 46 , 47 ].
Recently, Liu et al. Endothelial injury is emerging as a central hallmark of COVID pathogenesis, and the cytopathic virus can directly infect lung capillary endothelial cells that express ACE2 [ 54 , 56 ].
Intravascular microthrombi are the net result of an imbalance between procoagulant and fibrinolytic activity in the presence of acute inflammation and endothelial injury [ 45 , 57 , 58 , 59 ]. The pro-coagulant activity might result from complement system-mediated activation of clotting, similar to some forms of thrombotic microangiopathy TMA , or could be due to inhibition of plasminogen activation and fibrinolysis via increased activity of plasminogen activator inhibitor PAI-1 and -2 which are induced as acute-phase proteins under the influence of IL Autopsy of the lungs after severe disease showed fibrin deposition, diffuse alveolar damage, vascular wall thickening, and frequently occurring complement-rich microthrombi occluding lung capillaries and larger thrombi causing pulmonary artery thrombosis and embolism [ 63 , 64 , 65 ].
Moreover, coagulation is also modulated by activating C-reactive protein and ensuing complement activation and hepatic synthesis of fibrinogen as an acute phase protein in COVID [ 66 ]. Lung diffusion capacity DLCO can be impaired, although pure diffusion defects are rarely a cause for increased P A-a O 2 gradient at rest [ 67 , 68 ].
SARS-CoV-2 propagates within alveolar type II cells, where a large number of viral particles will be produced and released, followed by immune response mediated destruction of infected cells virus-linked pyroptosis [ 54 ].
Loss of alveolar epithelial cells and a pro-coagulant state cause the denuded basement membrane to be covered with debris, consisting of fibrin, dead cells, and complement activation products, collectively referred to as hyaline membranes [ 54 , 69 ].
With incremental exercise and in the face of absent hypoxic vasoconstriction in COVID, a hyperdynamic pulmonary circulation might not allow sufficient time for red blood cells to equilibrate their oxygen uptake.
Recently, Xiaoneng Mo et al. The prevalence of impaired diffusing-capacity was linked to the severity of disease, respectively The outline presented in the previous paragraphs largely clarifies the dissociation between the severity of hypoxemia in COVID and relatively well-preserved lung mechanics.
Gas exchange abnormalities in some patients with COVID occur earlier than increases in mechanical loads [ 41 ]. During the first days of infection, there is no increased airway resistance, and there is presumably no increased anatomical or physiological dead space ventilation. The breathing effort also remains rather low because lung compliance is normal in many patients without pre-existing lung disease.
As recently shown by Gattinoni et al. Such a wide discrepancy is highly unusual for most forms of disorders that lead to acute lung injury and ARDS [ 47 , 71 ]. Relatively high compliance indicates a well-preserved lung gas volume and explains in part the absence of dyspnea early in the course of illness [ 42 , 47 , 61 , 72 , 73 ].
In contrast, Ziehr et al. Of note, patients on mechanical ventilation have the highest COVID severity and thus probably the lowest respiratory system compliance. Dyspnea itself may have precipitated mechanical ventilation, and the latter may be a surrogate marker for low compliance in COVID [ 41 ]. Understanding of the respiratory mechanics found in COVID will continue to evolve as further research is reported. As the disease progresses, the more consolidated air spaces do not inflate as easily at higher transpulmonary pressures.
The volume loss is proportionally greater at higher lung volumes. This loss of volume reduces total lung compliance and increases the work of breathing [ 45 ].
There is also evidence that the dynamic compliance of the remaining ventilated lung is reduced in SARS-CoV-2 pneumonia as seen in pneumococcal pneumonia most possibly by a reduction in surfactant activity, further increasing the work of breathing [ 45 ]. Physiological dead space is also increasing due to reduced blood flow caused by intravascular thrombi. Importantly, the anxiety experienced by COVID patients also affects the cortical feedback to the respiratory centers. Consequently, as the disease progresses, dyspnea becomes increasingly apparent.
Regarding perfusion, avoiding microthrombi and ongoing fibrin deposition is one of the therapeutic strategies. It seems prudent to use thromboprophylaxis in all COVID patients, particularly in those with high D-dimers on admission [ 59 , 66 , 74 ]. Moore et al. In addition, tackling the systemic prothrombotic complication using anti-inflammatory medications such as anti-IL6R tocilizumab or sarilumab, or the anti-IL6 antibody siltuximab or complement inhibiting strategies to prevent macro- and microthrombi represents another potential approach and several trials are currently verifying this hypothesis [ 54 ].
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