text:
Internal Medicine/Dyspnea

DEFINITION AND EPIDEMIOLOGY
Dyspnea, colloquially known as "shortness of breath," is a multifaceted symptom that is characterized by breathing discomfort. It encompasses a spectrum of qualitatively distinct sensations and varies in intensity. This subjective experience is influenced by physiological, psychological, social, and environmental factors, often leading to secondary physiological and behavioral responses. It's essential to note that dyspnea is a symptom exclusively perceived and self-reported by the individual experiencing it, setting it apart from objective clinical signs such as tachypnea, accessory muscle use, or intercostal retraction, which can be quantified and reported by healthcare professionals.

The prevalence of dyspnea is notably high, and its impact on healthcare systems is substantial:

 * Approximately 50% of inpatients and 25% of ambulatory patients experience dyspnea during their medical encounters.
 * In the broader community, the prevalence ranges from 9% to 13%, with a significant increase to as high as 37% among adults aged 70 years or older.
 * Dyspnea ranks among the leading causes of emergency room visits, contributing to several million visits annually.
 * Its importance extends beyond sheer prevalence; dyspnea has emerged as a predictive marker in numerous chronic conditions, including chronic obstructive pulmonary disease (COPD), heart diseases, and various lung disorders.

MECHANISMS
Dyspnea is a complex phenomenon arising from diverse contributory respiratory sensations. To comprehend its mechanisms, one must consider the intricate interplay of physiological factors:

 * Afferent signals originating from peripheral chemoreceptors in the carotid body and aortic arch, as well as central chemoreceptors in the medulla, play a pivotal role. These receptors are sensitive to changes in oxygen levels (hypoxemia), carbon dioxide levels (hypercapnia), and acid-base balance (acidemia), potentially resulting in a sensation described as "air hunger."
 * Mechanoreceptors distributed throughout the upper airways, lungs (comprising stretch receptors, irritant receptors, and J receptors), and chest wall (including muscle spindles and tendon organs) can become activated in response to increased workloads within the respiratory system. This activation is associated with symptoms such as chest tightness, commonly observed in conditions like asthma or COPD, or reduced lung and chest wall compliance, as seen in pulmonary fibrosis.
 * Other afferent signals, stemming from pulmonary vascular receptors responding to changes in pulmonary artery pressure and skeletal muscle (referred to as metaboreceptors), contribute to the overall sensory experience of dyspnea.

In parallel, efferent signals originate from the central nervous system (CNS), specifically the motor cortex and brainstem, transmitting commands to the respiratory muscles. These efferent signals, accompanied by corollary discharge to the sensory cortex, underlie sensations of respiratory effort or "work of breathing." Additionally, fear or anxiety can exacerbate dyspnea by amplifying the underlying physiological disturbance, particularly during episodes of heightened respiratory rate or disordered breathing patterns.

ASSESSING DYSPNEA
Accurate assessment of dyspnea represents a significant challenge due to its multidimensional nature. There are multiple relevant domains to consider, including sensory-perceptual experience, affective distress, and symptom impact or burden. Although various tools have been developed for formal dyspnea assessment, consensus opinion leans toward tailoring the assessment to the context most relevant and beneficial for patient management. Furthermore, the specific domains being measured should be adequately described.

One example of a dyspnea assessment tool is the Modified Medical Research Council Dyspnea Scale. This scale, included in the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines, rates dyspnea on a scale from 0 to 4 based on the patient's self-reported level of breathlessness during different activities, helping to assess symptom/impact burden, particularly in COPD.

DIFFERENTIAL DIAGNOSIS
Dyspnea can manifest as a persistent symptom, lasting longer than one month, and can arise from a wide array of underlying conditions. Among the most common contributors are pulmonary and cardiac conditions, which together account for up to 85% of cases. However, it's crucial to recognize that up to one-third of patients may have multifactorial reasons underlying their dyspnea, making the diagnostic process challenging.

Here are some examples of conditions that underlie dyspnea, along with potential mechanisms and presenting symptoms:

 * Pulmonary System Causes: These encompass diseases of the airways (e.g., asthma and COPD), diseases of the lung parenchyma (e.g., interstitial lung diseases), chest wall disorders (e.g., kyphoscoliosis and neuromuscular weakness), and pulmonary vascular disorders (e.g., pulmonary hypertension). The associated symptoms may include chest tightness, tachypnea, increased work of breathing, air hunger, and an inability to take deep breaths.
 * Cardiovascular System Causes: Dyspnea can also result from conditions affecting the heart, such as coronary artery disease, cardiomyopathy, pericardial diseases (e.g., constrictive pericarditis and cardiac tamponade), or pulmonary vascular disorders like chronic thromboembolic disease. Symptoms may manifest as chest tightness, air hunger, or even left atrial myxoma, which leads to platypnea (dyspnea in an upright position relieved by lying down).
 * Other Causes: Dyspnea may originate from various factors, including anemia (reducing oxygen-carrying capacity), deconditioning (leading to increased perception of effort), and psychogenic factors (such as anxiety or panic disorders). These causes further emphasize the complexity of dyspnea evaluation.

The differential diagnosis process should be approached methodically, often necessitating a graded series of evaluations and investigations beginning with a thorough patient history and physical examination.

APPROACH TO THE PATIENT
The approach to a patient presenting with dyspnea depends on whether they have a known underlying condition or not. The primary objectives during evaluation are to determine whether the known condition has progressed or if a new etiology has emerged as the cause of dyspnea. For patients with known predisposing conditions, the evaluation seeks to assess disease progression. In contrast, for patients without a prior known potential cause of dyspnea, the initial evaluation focuses on identifying an underlying etiology, as this can significantly influence treatment decisions.

The evaluation process can be summarized as follows:

 * History and Physical Examination: An initial history and physical examination remain fundamental to the evaluation of dyspnea. It is essential to inquire about the patient's own description of the discomfort, its characteristics, and how it affects them. The physical examination should look for vital signs, including temperature, blood pressure, and heart rate, which may provide clues about the underlying etiology. Signs of increased work of breathing, such as supraclavicular retractions or use of accessory muscles, should be assessed. Other findings, such as anemia, cyanosis, or clubbing of the digits, may offer further diagnostic insights.
 * Diagnostic Testing: Based on the initial evaluation, diagnostic testing may be indicated to pinpoint the cause of dyspnea. This can include chest X-rays, spirometry, electrocardiograms, basic metabolic panels, and complete blood counts. Advanced tests like echocardiography, lung function testing, and CT angiography may be considered in specific cases.
 * Further Testing and Referral: In cases where the cause of dyspnea remains elusive, further testing and subspecialty referral to experts in pulmonology, cardiology, neurology, sleep medicine, or specialized dyspnea clinics may be necessary. As many as two-thirds of patients may require diagnostic testing beyond the initial clinical presentation.

DISTINGUISHING CARDIOVASCULAR FROM RESPIRATORY SYSTEM DYSPNEA
Distinguishing between cardiovascular and respiratory factors contributing to dyspnea is crucial for targeted and effective treatment. This differentiation can be achieved through a cardiopulmonary exercise test (CPET). CPET involves incremental symptom-limited exercise, often using cycling or treadmill protocols, while measuring key parameters such as ventilation, pulmonary gas exchange, heart rate, blood pressure, and oxygen consumption.

CPET results can provide critical insights:

 * If a patient reaches their predicted maximal ventilation during exercise, experiences increased dead space, or develops hypoxemia, it suggests that the respiratory system is primarily responsible for the exercise limitation.
 * Conversely, if the heart rate exceeds 85% of the predicted maximum, the anaerobic threshold is reached early, blood pressure becomes excessively high or drops during exercise, the O2 pulse (a measure of stroke volume) decreases, or there are ischemic changes on the electrocardiogram, it suggests an abnormality of the cardiovascular system as the main contributor to dyspnea during exercise.

Additionally, CPET can also help identify peripheral extraction deficits or underlying metabolic/neuromuscular diseases that might be driving dyspnea.

TREATMENT
Treatment of dyspnea primarily aims to correct underlying conditions or contributing factors, if possible. It is essential to address potentially reversible causes through targeted interventions. Given the multifactorial nature of dyspnea, multiple interventions may be necessary to address various aspects of the symptom.

Here are some key components of dyspnea management:

 * Correction of Underlying Conditions: The foremost goal is to treat the underlying conditions responsible for dyspnea. Effective management of conditions such as COPD, heart failure, interstitial lung disease, or pulmonary embolism can lead to significant symptom relief.
 * Supplemental Oxygen: For patients with resting oxygen saturation levels of 88% or lower or those experiencing significant desaturation during activity or sleep, supplemental oxygen can be beneficial. It helps improve oxygen delivery to tissues and alleviate dyspnea.
 * Pulmonary Rehabilitation: Programs focusing on pulmonary rehabilitation, including exercise training, education, and psychosocial support, have demonstrated positive effects on dyspnea, exercise capacity, and hospitalization rates. Some community-based programs, such as yoga and Tai Chi, can also be beneficial.
 * Opioids: In cases where dyspnea remains challenging to manage, opioids can be considered. They primarily reduce the sensation of air hunger, likely by suppressing respiratory drive and influencing cortical activity. However, opioid use should be carefully evaluated for each patient, considering the risk-benefit profile.
 * Anxiolytics: While anxiolytics have been explored for dyspnea management, their benefits have not consistently demonstrated across studies. Their use should be individualized, and potential side effects considered.
 * Emerging Approaches: Ongoing research is exploring innovative approaches to dyspnea management. Inhaled furosemide, for example, is under investigation and may alter afferent sensory information related to dyspnea.

Dyspnea remains a complex and challenging symptom, often necessitating a multidisciplinary approach to achieve optimal management. A deeper understanding of its mechanisms, accurate assessment, and targeted treatment strategies are crucial for improving the quality of life for individuals living with dyspnea.

MANAGEMENT OF CHRONIC BREATHLESSNESS SYNDROME (CBS)
Chronic breathlessness syndrome (CBS) represents a distinct entity within the realm of dyspnea. It is characterized by persistent breathlessness that endures despite optimal treatment of the underlying pathophysiology. Recognizing CBS is crucial as it necessitates a specific approach to symptom management.

Here are key aspects of managing CBS:

 * Comprehensive Evaluation: When dealing with CBS, it is imperative to conduct a comprehensive evaluation to identify any reversible contributing factors. This includes reviewing the patient's medical history, reevaluating underlying conditions, and reassessing the current treatment regimen.
 * Multidisciplinary Care: Given the complexity of CBS, a multidisciplinary approach is often necessary. This may involve collaboration between pulmonologists, cardiologists, palliative care specialists, and mental health professionals to address both physical and psychological aspects of the condition.
 * Symptom-Focused Interventions: Symptom management in CBS is centered on improving the patient's quality of life. This may involve pharmacological interventions, such as opioids or anxiolytics, to alleviate breathlessness and anxiety. However, these treatments should be carefully tailored to the individual patient and closely monitored for efficacy and side effects.
 * Psychosocial Support: CBS can have a profound impact on a patient's mental well-being. Providing psychosocial support, including counseling and therapy, can help patients cope with the distress associated with chronic breathlessness.
 * Patient Education: Educating patients and their caregivers about CBS, its course, and available management options is essential. Empowering patients with knowledge can lead to better self-management and improved overall outcomes.

RESEARCH AND FUTURE DIRECTIONS
Despite substantial progress in understanding dyspnea, there are ongoing research efforts aimed at advancing our knowledge and refining treatment strategies. Several areas of research and future directions include:

 * Neurobiology of Dyspnea: Further exploration of the neurobiological mechanisms underpinning dyspnea, including sensory and motor pathways, can provide valuable insights into potential therapeutic targets.
 * Precision Medicine: Advancements in genomics and personalized medicine may allow for tailored approaches to dyspnea management, accounting for genetic predispositions and individual variations in treatment responses.
 * Non-Pharmacological Interventions: Investigating the efficacy of non-pharmacological interventions, such as neuromodulation techniques or respiratory muscle training, can offer additional options for symptom relief.
 * Telemedicine and Remote Monitoring: Leveraging telemedicine and remote monitoring technologies can enhance the management of dyspnea, allowing for real-time assessment and intervention, particularly in chronic conditions.
 * Patient-Reported Outcomes: Incorporating patient-reported outcomes and preferences into dyspnea management can lead to more patient-centered care and improved treatment adherence.
 * Interdisciplinary Collaboration: Fostering collaboration among various medical specialties and researchers is crucial for a holistic understanding of dyspnea and the development of comprehensive management strategies.

In conclusion, dyspnea remains a multifaceted symptom with a profound impact on individuals' lives. It necessitates a holistic approach that considers its underlying mechanisms, accurate assessment, and tailored interventions. With ongoing research and a commitment to patient-centered care, there is hope for improved dyspnea management and enhanced quality of life for those affected by this challenging symptom.

title: Internal Medicine/Dyspnea


text:
Internal Medicine/Cough

Introduction to Cough
Cough, as a physiological response, plays a crucial role in safeguarding our respiratory system. It serves as a protective mechanism, helping to clear the airways and lungs of irritants, secretions, or foreign substances that might otherwise pose a threat to our respiratory health. Without an effective cough reflex, we would be at risk of retaining airway secretions and aspirating materials, potentially leading to infections, atelectasis (partial lung collapse), and respiratory compromise.

At the other end of the spectrum, excessive coughing can have detrimental effects. It can be exhausting, causing significant fatigue and discomfort. Prolonged or severe coughing episodes can lead to complications such as emesis (vomiting), syncope (fainting), muscular pain, or even rib fractures. In some cases, it can exacerbate pre-existing conditions like low back pain, abdominal or inguinal hernias, and urinary incontinence. Moreover, excessive coughing can be socially isolating, hindering normal interactions and causing discomfort to both the person with the cough and those around them.

Cough is often an early indicator of respiratory disease. In many instances, it manifests as an expected and accepted symptom of various respiratory conditions, especially during acute respiratory tract infections. However, when cough persists in the absence of other significant respiratory symptoms, it frequently prompts individuals to seek medical attention, signaling the potential presence of an underlying issue.

Understanding the Cough Mechanism
Coughing is not a simple reflex but a complex physiological process involving multiple sensory and motor components. It can be triggered by various stimuli, including both chemical and mechanical factors. Chemical stimuli, such as capsaicin, and mechanical factors, like mucus or particulates in air pollution, can initiate the cough reflex.

Sensory neuronal receptors, including cationic channels like transient receptor potential channels and adenosine triphosphate-activated ion channels (P2X3), play essential roles in detecting these stimuli. These receptors are primarily located in the pharynx, larynx, and airways, extending deep into the lung parenchyma. Interestingly, they can also be found in unexpected places, such as the external auditory canal and the esophagus.

The sensory signals from these receptors travel along the vagus and superior laryngeal nerves to a specific region in the brainstem known as the nucleus tractus solitarius. Here, integrated neural networks process the incoming signals, creating a conscious sensation referred to as the "urge to cough."

The efferent (outgoing) limb of the cough reflex involves a highly coordinated sequence of involuntary muscular actions. These actions include the adduction of the vocal cords, which leads to transient upper-airway occlusion. Concurrently, expiratory muscles contract, generating positive intrathoracic pressures that can reach as high as 300 mmHg. Upon the sudden release of laryngeal contraction, rapid expiratory flows are generated, surpassing the normal "envelope" of maximal expiratory flow observed on a flow-volume curve. Furthermore, bronchial smooth-muscle contraction, combined with dynamic airway compression, narrows airway lumens and maximizes the velocity of exhalation.

The kinetic energy generated by this forceful expiratory flow is critical for dislodging mucus from the inner walls of airways. This energy is directly proportional to the square of the velocity of expiratory airflow. Taking a deep breath before a cough optimizes the functioning of the expiratory muscles. In cases where multiple repetitive coughs occur at progressively lower lung volumes, they effectively sweep the point of maximal expiratory velocity further into the periphery of the lung.

Impaired Cough and Its Consequences
A weakened or ineffective cough can have serious consequences. It compromises the ability to clear lower respiratory tract secretions effectively, making individuals more susceptible to serious infections and their associated complications. When assessing cough strength, it is typically evaluated qualitatively, although objective measures such as peak expiratory flow or maximal expiratory pressure at the mouth can serve as surrogate markers for cough strength.

Various factors can contribute to impaired cough. These include weakness or paralysis of the expiratory muscles, as well as chest wall or abdominal pain. Chest wall deformities, like severe kyphoscoliosis, can also hinder the ability to produce an effective cough. Central respiratory depression, which can result from factors such as anesthesia, sedation, or neurological diseases, can further diminish cough strength.

Another critical aspect to consider is the nature of airway secretions. Abnormalities in secretions, such as abnormally viscous mucus seen in conditions like cystic fibrosis, can hinder effective clearance. Similarly, ciliary dysfunction, as seen in primary ciliary dyskinesia, or structural abnormalities of the airways, like tracheomalacia with excessive expiratory collapse of the trachea during cough, can all contribute to impaired cough function.

Symptomatic Cough and Its Diagnostic Significance
Cough often occurs in conjunction with other respiratory symptoms, which can collectively provide valuable clues for diagnosis. For instance, when cough is accompanied by wheezing, shortness of breath, and chest tightness following exposure to allergens like cat dander, it strongly suggests asthma as the underlying condition.

However, there are instances where cough takes center stage as the dominant or sole symptom of an underlying disease. In such cases, the duration and severity of the cough can offer retrospective insights into its potential etiology. Generally, cough can be categorized into three durations:

 * 1) Acute Cough (<3 weeks): Often associated with respiratory tract infections, aspiration events, or exposure to noxious chemicals or smoke.
 * 2) Subacute Cough (3–8 weeks): Commonly seen as a lingering symptom of tracheobronchitis, as in pertussis or "postviral tussive syndrome."
 * 3) Chronic Cough (>8 weeks): This form of cough can be attributed to a wide array of cardiopulmonary diseases, including inflammatory, infectious, neoplastic, and cardiovascular causes.

When a thorough initial assessment involving chest examination and radiography reveals no abnormalities, common identifiable causes of chronic cough include cough-variant asthma, gastroesophageal reflux, rhinosinusitis with excessive nasopharyngeal drainage, and medications like angiotensin-converting enzyme (ACE) inhibitors. In long-time cigarette smokers, a productive cough upon waking may suggest chronic bronchitis, while a dry, irritative cough persisting for more than two months after respiratory tract infections is often labeled as "postbronchitic cough."

However, it's worth noting that chronic cough can also manifest without an identifiable etiology. This intriguing phenomenon, recognized with increasing frequency, is believed to result from exaggerated neurologic signaling along sensory cough-reflex pathways. It is referred to as "chronic cough hypersensitivity syndrome."

Assessment of Chronic Cough
To arrive at a definitive diagnosis for chronic cough, a comprehensive approach is necessary. This includes both historical inquiries and a thorough physical examination. Key historical questions revolve around the circumstances surrounding the onset of cough, factors that exacerbate or alleviate the cough, and whether the cough produces sputum.

Physical examination plays a crucial role in identifying signs suggesting the presence of cardiopulmonary disease. Findings such as wheezing or crackles during chest examination, examination of the auditory canals and tympanic membranes to detect irritation stimulating Arnold's nerve, inspection of the nasal passages for signs of rhinitis or polyps, and examination of the nails for clubbing can all provide valuable etiologic clues. Additionally, because cough can sometimes be a manifestation of systemic diseases like sarcoidosis or vasculitis, a comprehensive general examination is equally important.

In nearly all instances, the evaluation of chronic cough should include a chest radiograph. This imaging modality is essential because the list of diseases capable of causing persistent cough without other symptoms and without detectable abnormalities on physical examination is extensive. It encompasses serious conditions such as sarcoidosis or Hodgkin's disease in young adults, lung cancer in older individuals, and, globally, pulmonary tuberculosis. If an abnormality is detected on the chest film, further evaluation is warranted to elucidate the cause of the radiographic anomaly.

In cases where chronic cough remains unexplained, despite a preserved ability to generate normal expiratory velocities, it's crucial to investigate other potential contributors. These can include abnormal airway secretions, ciliary dysfunction, or structural abnormalities of the airways, all of which can obstruct proper secretion clearance.

Chronic Cough with a Normal Chest Radiograph
It is a commonly held belief that certain factors, either alone or in combination, account for more than 90% of cases of chronic cough with a normal or noncontributory chest radiograph. These factors typically include the use of ACE inhibitors, postnasal drainage, gastroesophageal reflux, and asthma.

ACE inhibitor-induced cough, which occurs in 5–30% of patients taking these medications, is not dose-dependent. ACE inhibitors metabolize bradykinin and other tachykinins like substance P. The mechanism of ACE inhibitor-associated cough likely involves the sensitization of sensory nerve endings due to the accumulation of bradykinin. Therefore, any patient with chronic unexplained cough who is taking an ACE inhibitor should undergo a trial period without the medication, regardless of when the cough began relative to the initiation of ACE inhibitor therapy.

Postnasal drainage, which can occur due to various causes, can lead to cough as a response to the irritation of sensory receptors in the cough-reflex pathway located in the hypopharynx. Alternatively, aspiration of draining secretions into the trachea can also trigger cough. Physicians often refer to this condition as "upper airway cough syndrome." Common historical clues indicating postnasal drainage include a sensation of postnasal drip, frequent throat clearing, and symptoms like sneezing and rhinorrhea. On speculum examination of the nose, healthcare providers may observe excess mucoid or purulent secretions, inflamed and edematous nasal mucosa, and/or nasal polyps.

Linking gastroesophageal reflux to chronic cough presents similar challenges. It is hypothesized that reflux of gastric contents into the lower esophagus may initiate cough through reflex pathways originating in the esophageal mucosa. However, assessing reflux and its connection to cough is far from straightforward. Quantifying the frequency and extent of reflux necessitates somewhat invasive procedures, such as measuring esophageal pH or assessing esophageal pressures through manometry. The interpretation of test results and their ability to establish a direct link between reflux events and cough remains a matter of ongoing debate. Nevertheless, it's essential to balance the attribution of cough to gastroesophageal reflux with the understanding that many individuals with symptomatic reflux do not experience chronic cough.

Cough as the sole manifestation of asthma is more commonly observed in children than in adults. In such cases, it is referred to as "cough-variant asthma." Establishing this diagnosis typically involves a history suggestive of the onset of cough following exposure to known asthma triggers and the resolution of cough upon discontinuation of the trigger. Objective testing can help confirm or exclude asthma as the cause of cough. Such tests may include spirometry to detect airflow obstruction that varies over time or reverses in response to a bronchodilator. In cases where reliable measurements can be taken, home expiratory peak flow monitoring can be a cost-effective method to support or rule out an asthma diagnosis.

Eosinophilic bronchitis is another condition that can cause chronic cough, even when chest radiographs appear normal. This condition is characterized by sputum eosinophilia exceeding 3%, without evidence of airflow obstruction or bronchial hyperresponsiveness. The condition often responds positively to inhaled glucocorticoids. Measuring an elevated concentration of nitric oxide in exhaled breath has shown promise in detecting eosinophilic airway inflammation, potentially aiding in the diagnosis of conditions like asthma or eosinophilic bronchitis.

Symptom-Based Treatment of Cough
Treating chronic cough, especially in cases where no specific underlying cause has been identified, often involves empirical approaches targeting the most likely causes as determined by history, physical examination, and, occasionally, pulmonary function testing.

Postnasal Drainage: The treatment for cough due to postnasal drainage depends on the presumed etiology. In cases where infection, allergies, or vasomotor rhinitis are suspected, treatments may include systemic antihistamines, decongestants, antibiotics, nasal saline irrigation, and nasal pump sprays containing glucocorticoids, antihistamines, or anticholinergics.

Gastroesophageal Reflux: Addressing cough associated with gastroesophageal reflux disease (GERD) involves a multi-faceted approach. Antacids, histamine type 2 (H2) receptor antagonists, and proton pump inhibitors can help neutralize gastric acid or reduce its production. Lifestyle modifications such as dietary changes, elevating the head and torso during sleep, and medications that improve gastric emptying or impede the flow of refluxate (e.g., alginates) are additional therapeutic measures.

Cough-Variant Asthma: Patients with cough-variant asthma typically respond well to inhaled glucocorticoids and the intermittent use of inhaled β-agonist bronchodilators. These medications help manage the underlying inflammation and bronchial hyperresponsiveness that characterize asthma.

Cases That Defy Diagnosis: For individuals who do not respond to treatments targeting common causes of chronic cough or when these causes have been ruled out through appropriate diagnostic testing, it is advisable to consider a chest computed tomography (CT) scan. A chest CT can provide detailed imaging and reveal diseases that might not be evident on a chest x-ray. Such conditions may include early interstitial lung disease, bronchiectasis, tumors, or atypical mycobacterial pulmonary infections. Conversely, if a patient with chronic cough has normal findings on chest examination, lung function testing, oxygenation assessment, and chest CT, they can be reassured regarding the absence of serious pulmonary pathology.

Global Considerations in Cough
Cough is a symptom not limited to specific geographic regions, and its causes and management can vary based on environmental factors and prevalent diseases. In areas of the world where air pollution is a significant concern, exposure to pollutants can lead to chronic cough and throat clearing, along with lower respiratory tract diseases. Various forms of air pollution contribute to this issue, including smoke from cooking and heating fuels in poorly ventilated homes, toxic exposures in work environments lacking occupational safety standards, and ambient chemicals and particulates in highly polluted outdoor air.

Addressing cough related to air pollution focuses on improving environmental air quality. This can involve measures such as using stove chimneys in homes to reduce indoor smoke, implementing occupational safety standards in workplaces, and promoting the use of appropriate face masks in highly polluted outdoor areas.

In regions where tuberculosis is endemic, the presence of chronic cough raises concerns about active pulmonary tuberculosis. As such, healthcare providers must follow appropriate evaluation protocols, including chest imaging and sputum analysis, to promptly diagnose and treat cases of tuberculosis and prevent its spread.

Symptom-Based Treatment of Cough
Empirical treatment of chronic idiopathic cough has been explored using various medications, but consistent success remains elusive. Some of the medications that have been attempted include inhaled corticosteroids, inhaled anticholinergic bronchodilators, and macrolide antibiotics. However, their effectiveness in managing chronic cough has been inconsistent.

Currently available cough suppressants offer only modest relief. The most potent cough suppressants are narcotic medications like codeine, hydrocodone, or morphine. These drugs are believed to act directly on the "cough center" in the brainstem, reducing the urge to cough. However, their use is limited due to side effects such as drowsiness, constipation, and the potential for addictive dependence, making them less appealing for long-term use.

Dextromethorphan, an over-the-counter centrally acting cough suppressant, offers an alternative with fewer side effects than narcotic cough suppressants. It is believed to have a different site of action within the cough reflex pathway and can be used in combination with narcotic cough suppressants if necessary. Another option is benzonatate, which is thought to inhibit neural activity in the cough-reflex pathway. It is generally well-tolerated, but its effectiveness in suppressing cough can vary among individuals.

Inhaled lidocaine, which inhibits voltage-gated sodium channels, provides transient cough suppression. However, it carries the risk of oropharyngeal anesthesia, increasing the potential for aspiration.

Efforts to address cough hypersensitivity syndrome have primarily centered on inhibiting neural pathways. Small case series and randomized clinical trials have shown potential benefit from off-label use of medications like gabapentin, pregabalin, or amitriptyline. Recent studies have even suggested a role for behavioral modification using specialized speech therapy techniques. However, the widespread application of these therapies remains a challenge.

Future approaches to managing chronic cough involve the development of novel cough suppressants that do not possess the limitations of currently available agents. These approaches include the exploration of neurokinin-1 receptor antagonists, transient receptor protein vanilloid-1 (TRPV1) channel antagonists, a promising P2X3 channel antagonist known as gefapixant, and novel opioid and opioid-like receptor agonists.

Conclusion
Cough is a fascinating and complex physiological response with profound implications for our respiratory health and overall well-being. While it serves as a protective mechanism, its persistence or excessive manifestation can signal underlying medical issues that require careful evaluation and management. A comprehensive assessment, encompassing detailed patient history, physical examination, diagnostic imaging, and consideration of environmental factors, is essential to uncover the root causes of chronic cough and guide effective treatment strategies.

The management of chronic cough demands a patient-centered approach, considering individual factors, such as age, comorbidities, and medication tolerance. Despite the challenges posed by this symptom, ongoing research efforts continue to unravel the intricacies of cough physiology and pathology, offering hope for more effective and targeted treatments in the future. In the meantime, healthcare providers must remain vigilant in their pursuit of accurate diagnoses and symptom relief for those afflicted by chronic cough, understanding that each case presents a unique set of challenges and potential solutions.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

title: Internal Medicine/Cough


text:
Internal Medicine/Hemoptysis

Hemoptysis refers to the coughing up of blood from the respiratory tract. It can sometimes be confused with bleeding from the gastrointestinal tract (hematemesis) or the nose (epistaxis). In cases where hemoptysis is confirmed, the next step involves assessing the amount and frequency of blood expectoration. When the bleeding is massive or life-threatening (exceeding 400 mL of blood in 24 hours or 150 mL at one time), immediate intervention is necessary. This chapter primarily focuses on non-life-threatening cases of hemoptysis. Identifying the source and cause of the bleeding comes next when evaluating a patient with hemoptysis.

Anatomy and Physiology of Hemoptysis: Hemoptysis can originate anywhere within the respiratory tract, spanning from the glottis to the alveolus. Typically, bleeding occurs in the bronchi or medium-sized airways, but a comprehensive evaluation of the entire respiratory system is crucial. The lungs receive blood supply from both the pulmonary and bronchial circulations. While the pulmonary circulation serves gas exchange in the alveoli and is a low-pressure system, the bronchial circulation originates from the aorta and operates as a high-pressure system. Most hemoptysis cases arise from the bronchial circulation, and bleeding from this higher-pressure system can be challenging to control.

Etiology: Hemoptysis commonly results from infection, malignancy, or vascular disease. However, the potential causes of respiratory bleeding are diverse. In the United States, common causes include viral bronchitis, bronchiectasis, and malignancies. In other parts of the world, tuberculosis is a prevalent cause. Viral bronchitis typically leads to blood-tinged sputum and minor hemoptysis. Patients with chronic bronchitis are susceptible to bacterial superinfections, which can exacerbate airway inflammation and bleeding. Bronchiectasis, characterized by dilated, inflamed, and highly vascular airways, is a leading cause of massive hemoptysis.

Tuberculosis was historically the primary global cause of hemoptysis but has been surpassed by bronchitis and bronchiectasis in industrialized countries. In tuberculosis cases, bleeding often originates from cavitary disease, but complications like erosion of a pulmonary artery aneurysm into an existing cavity (Rasmussen's aneurysm) can also be the source.

Other infectious agents like endemic fungi, Nocardia, and nontuberculous mycobacteria can lead to cavitary lung disease with associated hemoptysis. Aspergillus species can form mycetomas within preexisting cavities, causing bleeding due to neovascularization. Pulmonary abscesses and necrotizing pneumonia can induce bleeding by damaging lung tissue. Common culprits include Staphylococcus aureus, Klebsiella pneumoniae, and oral anaerobes.

Paragonimiasis, a condition prevalent in Southeast Asia and China, can mimic tuberculosis and is a significant global cause of hemoptysis, even occurring in North America among recent immigrants.

Vascular causes of hemoptysis may be associated with cardiac issues, pulmonary embolism, arteriovenous malformations, or diffuse alveolar hemorrhage. While the classic description of pulmonary edema-related sputum is "pink and frothy," hemoptysis can also occur, particularly with the increased use of anticoagulants and antiplatelet medications.

Pulmonary embolism can lead to hemoptysis, but it is not a common cause. Ectatic vessels in airways or pulmonary arteriovenous malformations can also be sources of bleeding. A rare vascular cause is the rupture of an aortobronchial fistula, which arises in the context of aortic pathology like an aneurysm and can cause minor bleeding episodes that precede massive hemoptysis.

Diffuse alveolar hemorrhage (DAH) involves significant bleeding into lung tissue but is not typically associated with hemoptysis. DAH usually presents with diffuse ground glass opacities on chest imaging and can result from various factors, including immune-mediated capillaritis, toxicity from substances like cocaine, and stem cell transplantation.

While there is no universally agreed-upon volume, a blood loss of 400 mL in 24 hours or 100-150 mL at one time is considered life-threatening hemoptysis. These estimates are based on the blood volume within the tracheobronchial tree (generally 100-200 mL). Most patients do not accurately measure the volume of their hemoptysis in milliliters, so using approximations like cups (one U.S. cup is 236 mL) can be helpful. Thankfully, life-threatening hemoptysis only accounts for a small percentage of hemoptysis cases (5-15%).

A patient's medical history can provide clues to the cause of hemoptysis. Symptoms like fever, chills, or a prior cough may suggest an infection. Smoking history or unintentional weight loss may increase suspicion of malignancy. Patients should also be questioned about inhalational exposures, including vaping. A thorough medical history, with special attention to chronic pulmonary diseases and risk factors for malignancy and bronchiectatic lung disease (e.g., cystic fibrosis, sarcoidosis), is essential.

Physical Examination: Reviewing vital signs is the first step in assessing a patient with hemoptysis. Those with life-threatening hemoptysis can exhibit hypoxemia, tachycardia, and hemodynamic instability. Evaluating the nasal and oral cavities is crucial to identify any potential sources of bleeding. Additionally, listening to the lungs and searching for other relevant physical findings such as clubbing can help pinpoint the cause of hemoptysis. Wheezing in a specific area may indicate foreign body aspiration. Signs of a bleeding diathesis, like skin or mucosal ecchymoses and petechiae, or the presence of telangiectasias may suggest other underlying causes of hemoptysis.

Diagnostic Studies: Initial diagnostic studies should encompass a complete blood count to assess for signs of infection, anemia, or thrombocytopenia; coagulation parameters; electrolyte and renal function measurements; and urinalysis to rule out pulmonary-renal disease. Chest imaging is a crucial component of the evaluation for every patient.

A chest radiograph is typically the first imaging modality employed, although it may not always localize the bleeding source and can appear normal in some cases. Patients without risk factors for malignancy or other abnormalities in their initial evaluation and with a normal chest radiograph may be treated for bronchitis with close follow-up, as it represents a reasonable strategy in such cases. Conversely, patients with risk factors for malignancy (e.g., age over 40 or a history of smoking) should undergo further testing. This often includes contrast-enhanced chest computed tomography (CT) to better identify masses, bronchiectasis, and parenchymal lesions. A CT scan to check for pulmonary embolism may also be considered if the patient's history and physical examination align with that diagnosis. After a CT scan, a flexible bronchoscopy is usually performed to exclude bronchogenic carcinoma unless imaging reveals a lesion that can be sampled without bronchoscopy. Small case series suggest that patients with hemoptysis and unremarkable bronchoscopies tend to have favorable outcomes.

Interventions: In cases where hemoptysis is massive or life-threatening, three simultaneous goals must be pursued: protecting the nonbleeding lung, identifying the site of bleeding, and controlling the bleeding.

Protecting the airway and the nonbleeding lung is of utmost importance when managing massive hemoptysis, as asphyxiation can occur rapidly. If the bleeding site is known, positioning the patient with the bleeding side down can help prevent blood from entering the nonbleeding lung. Endotracheal intubation should be reserved for cases where it is absolutely necessary, as suctioning through an endotracheal tube is less effective than the cough reflex in removing blood and clots. If intubation becomes necessary, steps should be taken to protect the nonbleeding lung, either through selective intubation of one lung (the nonbleeding one) or the use of a double-lumen endotracheal tube.

Identifying the bleeding site can be straightforward in some cases but challenging in others. A chest radiograph can provide some localization information if it shows new opacities, although it is not sufficient on its own. CT angiography can be helpful by pinpointing active extravasation. Flexible bronchoscopy may aid in identifying the side of bleeding, although it has a 50% chance of success at best. Experts do not universally agree on the timing of bronchoscopy; in some cases, such as cystic fibrosis, it may not be recommended, as it could delay definitive management. Proceeding directly to angiography is also a reasonable strategy, as it offers both diagnostic and therapeutic capabilities.

Controlling bleeding during a life-threatening episode of hemoptysis can be achieved in one of three ways: from the airway lumen, from the involved blood vessel, or through surgical resection of both the affected airway and vessel. Bronchoscopic measures are generally temporary solutions. A flexible bronchoscope can be used to remove clots and insert a balloon catheter or bronchial blocker to block the affected airway temporarily. Rigid bronchoscopy, performed by an interventional pulmonologist or thoracic surgeon, may enable therapeutic interventions for bleeding airway lesions, such as photocoagulation and cautery. Since most life-threatening hemoptysis cases arise from the bronchial circulation, bronchial artery embolization is the preferred procedure for controlling bleeding. However, bronchial artery embolization can carry significant complications, such as embolization of the anterior spinal artery. Nevertheless, it is generally effective in the short term, with a success rate of over 80% in immediately controlling bleeding, although recurrence is possible if the underlying disease (e.g., a mycetoma) is not treated. Surgical resection should be considered only if initial measures fail and bleeding persists. Ideal candidates for surgery have localized disease but otherwise normal lung tissue.

Summary of Approach to Hemoptysis Management:
 * 1) History and Examination: The initial assessment involves gathering a detailed patient history and conducting a physical examination. The history should include inquiries about the amount and characteristics of the bleeding, associated symptoms, risk factors, smoking history, and possible inhalational exposures. Vital signs, including oxygen saturation, heart rate, and blood pressure, should be reviewed. Examination should focus on identifying signs of active bleeding, the source of bleeding, and other relevant physical findings.
 * 2) Diagnostic Studies: Depending on the patient's history and risk factors, initial diagnostic studies may include:
 * 3) * Complete blood count (CBC) to assess for infection, anemia, or thrombocytopenia.
 * 4) * Coagulation parameters to evaluate the patient's clotting function.
 * 5) * Measurement of electrolytes and renal function.
 * 6) * Urinalysis to exclude pulmonary-renal disease.
 * 7) * Chest imaging, typically starting with a chest radiograph, which may be followed by contrast-enhanced chest computed tomography (CT) in high-risk patients.
 * 8) Interventions: The approach to managing hemoptysis depends on the severity of bleeding:
 * 9) * In cases of nonmassive hemoptysis without risk factors, treating the underlying cause (usually infection) may suffice.
 * 10) * In massive or life-threatening hemoptysis, immediate action is essential:
 * 11) ** Protecting the airway and the nonbleeding lung is a priority. The patient may be positioned with the bleeding side down, and endotracheal intubation should be considered if necessary.
 * 12) ** Identifying the bleeding site may require imaging modalities like CT angiography or flexible bronchoscopy.
 * 13) ** Controlling bleeding can be achieved through bronchoscopic measures, bronchial artery embolization, or, as a last resort, surgical resection.
 * 14) Bronchoscopy: Flexible bronchoscopy can help visualize and locate the bleeding source in the airways. However, its success rate in identifying the site is limited.
 * 15) Bronchial Artery Embolization: This is the preferred method for controlling bleeding in cases where hemoptysis originates from the bronchial circulation. It involves blocking the bronchial arteries that supply the bleeding area, effectively stopping the bleeding.
 * 16) Surgical Resection: Surgical removal of the affected airway and vessel is considered in cases where initial measures fail, and bleeding persists. This is a high-risk procedure and is typically reserved for localized disease with otherwise normal lung tissue.

Conclusion: Hemoptysis, or the coughing up of blood from the respiratory tract, can have various causes, including infection, malignancy, and vascular issues. Proper evaluation and management are crucial, with a focus on protecting the airway, identifying the bleeding source, and controlling the bleeding. The approach to management depends on the severity of hemoptysis, with massive or life-threatening cases requiring urgent intervention, including bronchial artery embolization or surgical resection in extreme cases. Early diagnosis and appropriate treatment are essential for the successful management of hemoptysis.

title: Internal Medicine/Hemoptysis


text:
Internal Medicine/Hypoxia and Cyanosis

Hypoxia

 * Purpose of the Cardiorespiratory System
 * The primary function of the cardiorespiratory system is to ensure the delivery of oxygen (O2) and nutrients to cells while removing carbon dioxide (CO2) and metabolic waste products from them. This vital process relies not only on the integrity of the cardiovascular and respiratory systems but also on factors like red blood cell count, hemoglobin levels, and the availability of inspired air with sufficient oxygen content.
 * Responses to Hypoxia
 * Hypoxia, which signifies decreased O2 availability to cells, leads to significant metabolic changes. It typically results in the inhibition of oxidative phosphorylation and an increase in anaerobic glycolysis. This shift from aerobic to anaerobic metabolism, known as the Pasteur effect, reduces the rate of adenosine 5'-triphosphate (ATP) production.
 * In severe hypoxia, when ATP production falls short of meeting cellular energy demands, it triggers cell membrane depolarization, uncontrolled calcium ion (Ca2+) influx, and the activation of Ca2+-dependent enzymes, ultimately leading to cell swelling, activation of apoptotic pathways, and cell death.
 * The body adapts to hypoxia by upregulating genes that encode various proteins, including glycolytic enzymes like phosphoglycerate kinase and phosphofructokinase, as well as glucose transporters (Glut-1 and Glut-2). Growth factors such as vascular endothelial growth factor (VEGF) and erythropoietin enhance red blood cell production. Hypoxia-induced gene expression is largely governed by the hypoxia-sensitive transcription factor, hypoxia-inducible factor-1 (HIF-1).
 * Hypoxia also induces systemic arteriolar dilation by opening KATP channels in vascular smooth muscle cells, due to a decrease in ATP concentration. In contrast, in pulmonary vascular smooth muscle cells, inhibition of potassium (K+) channels leads to depolarization, activating voltage-gated Ca2+ channels, raising cytosolic Ca2+ levels, and causing smooth muscle contraction. While this hypoxia-induced pulmonary arterial constriction diverts blood from poorly ventilated lung areas to better-ventilated ones, it increases pulmonary vascular resistance and right ventricular afterload.
 * Hypoxia's effects on the Central Nervous System (CNS) are significant. Acute hypoxia results in impaired judgment, motor coordination, and symptoms resembling acute alcohol intoxication. High-altitude illness includes symptoms like headaches, gastrointestinal distress, dizziness, insomnia, and fatigue. Severe hypoxia can lead to high-altitude pulmonary edema (HAPE) or, rarely, high-altitude cerebral edema (HACE), which can cause severe headaches, papilledema, and coma. In the later stages of severe hypoxia, brainstem regulatory centers are affected, typically leading to respiratory failure and death.
 * In the Cardiovascular System, acute hypoxia triggers the chemoreceptor reflex, causing venoconstriction and systemic arterial vasodilation. This initial response is accompanied by a transient increase in myocardial contractility, followed by decreased contractility with prolonged hypoxia.
 * Causes of Hypoxia
 * Respiratory Hypoxia: It occurs due to respiratory failure, causing a decline in arterial oxygen partial pressure (Pao2). In cases of persistent respiratory failure, the hemoglobin-oxygen (Hb-O2) dissociation curve shifts to the right, leading to arterial hypoxemia, especially when caused by pulmonary diseases.
 * Hypoxia Secondary to High Altitude: As individuals ascend to high altitudes, the reduced oxygen content in inspired air (Fio2) decreases alveolar oxygen partial pressure (Pao2). This leads to high-altitude illness, characterized by symptoms like headache, gastrointestinal issues, and more severe hypoxemia at higher altitudes.
 * Hypoxia Secondary to Right-to-Left Extrapulmonary Shunting: This type of hypoxia is similar to intrapulmonary right-to-left shunting but is due to congenital cardiac malformations, such as tetralogy of Fallot or atrial septal defects.
 * Anemic Hypoxia: It results from reduced hemoglobin concentration in the blood, leading to decreased oxygen-carrying capacity. Even though Pao2 may be normal, the absolute amount of O2 transported per unit of blood volume is reduced.
 * Carbon Monoxide (CO) Intoxication: Hemoglobin binding with CO (carboxy-hemoglobin [COHb]) limits O2 transport, and COHb shifts the Hb-O2 dissociation curve to the left, reducing O2 unloading, further contributing to tissue hypoxia.
 * Circulatory Hypoxia: Occurs due to reduced tissue perfusion and increased tissue O2 extraction, leading to an increased arterial-mixed venous O2 difference (a-v-O2 difference). It is common in heart failure and various forms of shock.
 * Specific Organ Hypoxia: Localized circulatory hypoxia can result from arterial obstruction, vasoconstriction, venous obstruction, or edema. Different organs can experience localized hypoxia for various reasons.
 * Increased O2 Requirements: Elevated tissue O2 consumption without a corresponding increase in perfusion leads to tissue hypoxia and a decline in venous Po2.
 * Improper Oxygen Utilization: Certain toxins, like cyanide, impair cellular O2 utilization by interfering with mitochondrial electron transport and oxidative phosphorylation, leading to histotoxic hypoxia.
 * Adaptation to Hypoxia
 * The body responds to chronic hypoxia by increasing hemoglobin concentration and red blood cell production in the bloodstream, known as polycythemia. Chronic mountain sickness is a condition that can develop in individuals exposed to prolonged high-altitude hypoxemia, characterized by a blunted respiratory drive, reduced ventilation, erythrocytosis, and other symptoms.

Cyanosis

 * Definition and Types of Cyanosis
 * Central Cyanosis: Occurs when arterial oxygen saturation (Sao2) decreases significantly, usually due to reduced oxygen partial pressure (Pao2). It is often associated with respiratory or cardiovascular problems.
 * Peripheral Cyanosis: Typically caused by normal vasoconstriction in response to cold exposure. It may also result from reduced cardiac output, arterial obstruction, venous obstruction, or other circulatory issues.
 * Differential Diagnosis of Central Cyanosis: Various factors can cause central cyanosis, including low Pao2 due to reduced atmospheric pressure, impaired pulmonary function (e.g., pneumonia or pulmonary edema), anatomic shunts (e.g., certain congenital heart diseases), and more.
 * Approach to the Patient with Cyanosis:
 * Evaluating the time of onset, differentiating central from peripheral cyanosis, checking for clubbing of the digits, measuring Pao2 and Sao2, and conducting spectroscopic examination of blood when the cause of cyanosis is unclear.
 * Clubbing:
 * Clubbing is the bulbous enlargement of distal finger and toe segments due to connective tissue proliferation. It can be hereditary, idiopathic, or associated with various medical conditions, including congenital heart disease, lung diseases (e.g., lung cancer, bronchiectasis), gastrointestinal diseases (e.g., inflammatory bowel disease, hepatic cirrhosis), and certain occupational exposures.

title: Internal Medicine/Hypoxia and Cyanosis


text:
Internal Medicine/Edema

Introduction to Edema
Edema is a prevalent clinical manifestation characterized by the abnormal accumulation of fluid in the interstitial spaces within the body. It can occur as a result of numerous underlying medical conditions, and its severity can range from mild swelling to severe fluid retention. Understanding the specific causes and mechanisms of edema is crucial for effective diagnosis and management.

Generalized Edema
Generalized edema is a term used to describe edema that affects the entire body or large areas of the body, as opposed to being confined to a specific region. This type of edema is often associated with systemic medical conditions and can be a sign of underlying health issues. Generalized edema may manifest as swelling in the legs, ankles, hands, face, or even throughout the entire body.

Cardiac Causes of Generalized Edema
One of the primary causes of generalized edema is heart failure. In heart failure, the heart's ability to pump blood effectively is compromised. As a result, fluid accumulates in the venous circulation, leading to increased venous and intracapillary pressure. This excess fluid eventually leaks into the surrounding tissues, causing edema. Additionally, the activation of neurohumoral mechanisms, such as the renin-angiotensin-aldosterone system (RAAS), exacerbates sodium and water retention, further contributing to edema.

Hepatic Causes of Generalized Edema
Hepatic cirrhosis is another significant contributor to generalized edema. This condition is characterized by hepatic venous outflow obstruction, which, in turn, causes an expansion of splanchnic (abdominal) blood volume and hepatic lymph formation. Intrahepatic hypertension stimulates renal sodium retention and leads to a reduction in effective arterial blood volume. Furthermore, hepatic cirrhosis often results in hypoalbuminemia due to decreased hepatic synthesis and peripheral arterial vasodilation. These combined effects trigger the retention of sodium and water, contributing to the development of edema.

Renal Causes of Generalized Edema
Generalized edema can also arise from renal disorders. In cases of acute glomerulonephritis, edema typically accompanies symptoms such as hematuria, proteinuria, and hypertension. This form of edema primarily results from the impaired ability of the kidneys to regulate sodium and water balance. Unlike heart failure, glomerulonephritis is characterized by a normal or even increased cardiac output.

Chronic renal failure (CRF) is another renal condition associated with generalized edema. In CRF, there may be signs and symptoms of uremia, such as decreased appetite, altered taste, sleep disturbances, difficulty concentrating, and even myoclonus. Elevated blood pressure, hypertensive retinopathy, and nitrogenous fetor (an ammonia-like odor to the breath) may also be present. Laboratory findings in CRF often include increased serum creatinine and cystatin C levels, albuminuria, hyperkalemia, metabolic acidosis, hyperphosphatemia, hypocalcemia, and anemia.

Other Causes of Generalized Edema
Various other factors can contribute to generalized edema. Medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs), antihypertensive agents, vasodilators, and certain hormones (glucocorticoids, anabolic steroids, estrogens, progestins), may lead to fluid retention. These drugs can affect renal function, vascular tone, or capillary permeability.

Nutritional deficiencies, particularly those resulting from a diet deficient in calories and protein over an extended period, can lead to hypoproteinemia and edema. Beriberi heart disease, a nutritional disorder, may also intensify edema due to the development of peripheral arteriovenous fistulae, reducing systemic perfusion and effective arterial blood volume.

Localized Edema
In contrast to generalized edema, localized edema occurs in specific areas of the body. Common causes of localized edema include conditions like thrombophlebitis, varicose veins, and primary venous valve failure. These conditions increase hydrostatic pressure in the capillary bed upstream of the obstruction, causing abnormal fluid transfer from the vascular to the interstitial space, resulting in localized swelling.

Additionally, localized edema may arise from lymphatic obstruction due to chronic lymphangitis, surgical resection of regional lymph nodes, filariasis, or genetic (primary) lymphedema. Primary lymphedema, often hereditary, presents a unique challenge because it restricts lymphatic flow, leading to increased intracapillary pressure and protein concentration in the interstitial fluid, which exacerbates fluid retention.

Distribution of Edema
The distribution of edema throughout the body can provide essential diagnostic clues. For example, in heart failure, edema tends to be more prominent in the lower extremities, especially the legs, and may worsen in the evening due to posture-related factors. Patients with heart failure who are confined to bed may develop edema primarily in the presacral region.

In contrast, edema resulting from hypoalbuminemia, as seen in the nephrotic syndrome, is typically generalized. However, it is most noticeable in the soft tissues of the face and eyelids, often being most pronounced in the morning after a night of recumbent posture. Facial edema can also occur in other conditions like trichinosis, allergic reactions, and myxedema.

Edema limited to one limb or affecting one or both arms is typically associated with venous and/or lymphatic obstruction. Unilateral paralysis can reduce lymphatic and venous drainage on the affected side, potentially causing unilateral edema. In cases of superior vena cava obstruction, edema is confined to the face, neck, and upper extremities due to elevated venous pressure in these areas.

Approach to the Patient with Edema
When evaluating a patient with edema, it is crucial to determine whether the edema is localized or generalized. If generalized, several key steps should be taken:

 * Assess serum albumin levels: Hypoalbuminemia (serum albumin <3.0 g/dL) may indicate underlying conditions such as cirrhosis, severe malnutrition, or the nephrotic syndrome.
 * Gather a detailed medical history: This should include information about the patient's medical conditions, medications, dietary habits, and any recent changes in health.
 * Conduct a thorough physical examination: Pay attention to signs of cardiac, hepatic, or renal dysfunction, as well as any localized causes of edema.
 * Perform urinalysis and additional laboratory tests: These can help evaluate kidney function, proteinuria, electrolyte imbalances, and other factors contributing to edema.
 * Monitor urine output: Assess whether the patient has an adequate urine output, oliguria (reduced urine production), or anuria (complete absence of urine production).

By following this systematic approach, healthcare providers can work towards identifying the underlying cause of edema and developing an appropriate treatment plan.

title: Internal Medicine/Edema


text:
Internal Medicine/Heart Murmur

Introduction to Cardiac Murmurs
Cardiac murmurs are common findings in clinical practice and can result from various cardiac and vascular abnormalities. These murmurs are often detected during auscultation, the process of listening to the heart sounds using a stethoscope. Heart murmurs can be indicative of underlying structural or functional issues within the heart, making their evaluation a crucial aspect of diagnosing and managing cardiovascular conditions.

Systolic Heart Murmurs
Systolic heart murmurs occur during ventricular systole, the phase of the cardiac cycle when the ventricles contract and pump blood into the aorta and pulmonary artery. These murmurs are characterized by their timing, location, radiation, intensity, and pitch. Common causes of systolic murmurs include:

 * Aortic Stenosis: This condition involves the narrowing of the aortic valve opening, causing turbulence as blood is forced through the constricted valve.
 * Hypertrophic Cardiomyopathy: In hypertrophic cardiomyopathy, the heart muscle becomes abnormally thick, leading to turbulent blood flow and a characteristic systolic murmur.
 * Mitral Regurgitation: This condition occurs when the mitral valve does not close properly during systole, allowing blood to flow backward into the left atrium.
 * Ventricular Septal Defects (VSD): VSDs are congenital heart defects where there is an abnormal communication between the right and left ventricles, resulting in a murmur due to the shunting of blood.

Diastolic Heart Murmurs
Diastolic heart murmurs occur during ventricular diastole, the phase when the ventricles relax and fill with blood. These murmurs are also characterized by timing, location, intensity, and pitch. Common causes of diastolic murmurs include:

 * Aortic Regurgitation: In aortic regurgitation, the aortic valve does not close properly during diastole, allowing blood to leak back into the left ventricle.
 * Mitral Stenosis: This condition involves the narrowing of the mitral valve, obstructing the flow of blood from the left atrium to the left ventricle.
 * Pulmonic Regurgitation: Pulmonic regurgitation occurs when the pulmonic valve does not close tightly during diastole, causing blood to flow back into the right ventricle.

Continuous Murmurs
Continuous murmurs are unique in that they span both systole and diastole, starting in systole and extending into part or all of diastole. These murmurs are characterized by their persistence and can be associated with specific conditions, including:

 * Patent Ductus Arteriosus: This congenital heart defect involves a persistent connection between the aorta and the pulmonary artery, creating a continuous pressure gradient throughout the cardiac cycle, resulting in a continuous murmur.
 * Ruptured Sinus of Valsalva Aneurysm: In this condition, there is a rupture in one of the sinuses of Valsalva, leading to turbulent blood flow and a continuous murmur.
 * Coronary Arteriovenous Fistula: This anomaly involves an abnormal connection between a coronary artery and a cardiac chamber or blood vessel, resulting in continuous blood flow and a continuous murmur.

Dynamic Auscultation
Dynamic auscultation involves observing changes in the intensity and characteristics of heart murmurs during specific maneuvers. These maneuvers include:

 * Respiration: Changes in intrathoracic pressure during breathing can affect venous return and may impact the intensity of certain murmurs.
 * Isometric Exercise (Handgrip): Sustained handgrip can alter left ventricular afterload and affect the loudness of murmurs, particularly those associated with mitral regurgitation and ventricular septal defects.
 * Transient Arterial Occlusion: Inflating blood pressure cuffs on both upper extremities can temporarily alter systemic blood pressure and influence murmur intensity.
 * Pharmacologic Manipulation: The administration of vasopressor agents or inhaled amyl nitrite can modulate systemic vascular resistance and affect the loudness of certain murmurs.

 * Valsalva Maneuver: The Valsalva maneuver involves increasing intrathoracic pressure followed by a decrease in venous return, ventricular filling, and cardiac output. Most murmurs decrease in intensity during the strain phase of the Valsalva maneuver, except for those associated with Mitral Valve Prolapse (MVP) and Hypertrophic Obstructive Cardiomyopathy (HOCM), which become louder.
 * Rapid Standing/Squatting: Abrupt changes in posture from squatting to standing can affect venous return and left ventricular afterload, impacting the intensity and timing of murmurs.
 * Passive Leg Raising: This maneuver can be used to increase venous return in patients who cannot perform squatting and standing. It may affect the intensity of certain murmurs, particularly those associated with HOCM.
 * Post-Premature Ventricular Contraction: A change in the intensity of a systolic murmur in the beat following a premature ventricular contraction (PVC) can help distinguish Aortic Stenosis (AS) from Mitral Regurgitation (MR). Systolic murmurs due to left ventricular outflow obstruction, such as AS, increase in intensity in the beat after a PVC, while the intensity of the murmur of MR remains relatively stable.

The Clinical Context
In addition to auscultation and dynamic maneuvers, an accurate assessment of heart murmurs involves considering the clinical context and other physical examination findings. Key factors to consider include:

 * Symptoms: Symptoms suggestive of cardiovascular, neurologic, or pulmonary disease can provide important clues to the etiology and significance of a heart murmur.
 * Associated Findings: Findings relevant to the jugular venous pressure, arterial pulses, other heart sounds (e.g., S1, S2, S3, S4), lung sounds, abdominal findings, skin findings, and extremity findings can aid in the differential diagnosis.
 * Laboratory Studies: Results from laboratory studies, electrocardiograms (ECGs), and chest X-rays obtained earlier in the evaluation may contain valuable information to help assess the cause of a heart murmur.
 * Clinical Syndromes: Recognizing clinical syndromes, such as infective endocarditis or myocardial rupture following a myocardial infarction, can provide important diagnostic insights.

Echocardiography
Echocardiography is a valuable diagnostic tool for the assessment of cardiac murmurs. This non-invasive imaging technique provides detailed information about cardiac structure and function, including:

 * Valve Structure and Function: Echocardiography can assess the condition and function of heart valves, identifying issues such as stenosis or regurgitation.
 * Chamber Size and Wall Thickness: The size and thickness of cardiac chambers can be measured, aiding in the diagnosis of conditions like hypertrophic cardiomyopathy.
 * Ventricular Function: Echocardiography allows for the evaluation of left and right ventricular function.
 * Pulmonary Artery Pressures: Estimated pulmonary artery pressures can be determined.
 * Intracardiac Shunt Flow: Echocardiography can detect intracardiac shunts, such as atrial septal defects (ASD) or ventricular septal defects (VSD).
 * Aortic and Pulmonary Flow: The flow of blood through the aorta and pulmonary artery can be assessed.

Other Cardiac Testing
In some cases, additional cardiac testing may be necessary to fully evaluate heart murmurs. This includes:

 * Transesophageal Echocardiography (TEE): TEE can provide enhanced sensitivity in cases where transthoracic echocardiography (TTE) is limited by patient factors or anatomy.
 * Cardiac Magnetic Resonance (CMR) Imaging: CMR provides quantitative information about valvular function, ventricular size, and myocardial perfusion. It is particularly useful when there is a discrepancy between clinical and echocardiographic findings.
 * Cardiac CT: Cardiac CT can help assess aortic valve anatomy and exclude coronary artery disease in certain patients before valve surgery.
 * Invasive Angiography and Hemodynamic Assessment: In some cases, invasive angiography and hemodynamic assessment may be required for a comprehensive preoperative evaluation.

Integrated Approach
The accurate identification and evaluation of heart murmurs involve a systematic approach that integrates findings from cardiac auscultation, clinical history, physical examination, and various diagnostic tests. The need for further testing should be determined based on the specific characteristics of the murmur and the clinical context. Cost-effectiveness and the potential impact on patient outcomes should guide decisions regarding non-invasive imaging.

In summary, heart murmurs are important clinical signs that can indicate underlying cardiac conditions. A comprehensive evaluation, including dynamic auscultation, echocardiography, and additional testing when needed, allows healthcare providers to diagnose and manage these conditions effectively.

title: Internal Medicine/Heart Murmur


text:
Internal Medicine/Palpitations

Palpitations are a common complaint among patients when they visit their internists. These are often described as sensations of "thumping," "pounding," or "fluttering" in the chest. Palpitations can vary in frequency and regularity, and many patients become concerned when they feel their heartbeats skip or miss a beat. These sensations are often noticed during moments of rest when external stimuli are minimal. When palpitations are positional, they may be linked to structural issues within or near the heart, such as atrial myxoma or mediastinal masses.

The causes of palpitations can be broadly categorized into cardiac (43%), psychiatric (31%), miscellaneous (10%), and unknown (16%) factors. Cardiovascular causes include premature contractions of the atria and ventricles, various arrhythmias, mitral valve prolapse, aortic insufficiency, atrial myxoma, myocarditis, and pulmonary embolism. Intermittent palpitations are frequently associated with premature contractions of the atria or ventricles, where the post-extrasystolic beat is felt due to changes in the heart's rhythm. Regular, sustained palpitations can result from consistent supraventricular and ventricular tachycardias, while irregular, sustained palpitations may be caused by atrial fibrillation. It's important to note that most arrhythmias do not lead to palpitations, but when they do, patients can help by tapping out the rhythm or checking their pulse during episodes.

Certain factors, such as exercise, stress, or substances like tobacco, caffeine, and drugs, can lead to hyperdynamic cardiovascular states and palpitations. Athletes and individuals with conditions like aortic regurgitation may also experience palpitations due to increased myocardial contraction strength. Psychiatric causes, such as panic attacks, anxiety, and somatization, can lead to palpitations, often with longer durations and accompanying symptoms.

When assessing patients with palpitations, the primary goal is to determine if a life-threatening arrhythmia is the cause. Patients with coronary artery disease (CAD) or CAD risk factors are at higher risk for ventricular arrhythmias. Additional symptoms like syncope or lightheadedness can support this diagnosis. A thorough physical examination, measurement of vital signs, assessment of jugular venous pressure, pulse evaluation, and chest auscultation can help confirm or rule out an arrhythmia. Resting electrocardiograms are useful for documenting arrhythmias, while exercise electrocardiography can help if arrhythmias are exercise-induced. For infrequent arrhythmias, various monitoring methods like Holter monitoring, telephonic monitoring, loop recordings, and mobile cardiac outpatient telemetry can be employed.

Most patients with palpitations do not have serious arrhythmias or structural heart issues. Benign atrial or ventricular premature contractions can often be managed with beta-blocker therapy if necessary. Palpitations triggered by alcohol, tobacco, or illicit drugs require abstinence, and those caused by medications should be addressed by considering alternative treatments. Psychiatric causes of palpitations may benefit from cognitive therapy or medication. It's important for physicians to recognize that palpitations can be distressing to patients, but once serious causes are ruled out, patients should be reassured that their prognosis is not adversely affected by palpitations.

title: Internal Medicine/Palpitations


text:
Internal Medicine/Dysphagia

Definition and Classification
Dysphagia is a complex condition, and understanding its nuances requires categorization. It can be broadly classified into two main types: oropharyngeal dysphagia and esophageal dysphagia.

 * Oropharyngeal dysphagia primarily involves difficulties in the initial phases of swallowing, typically from the mouth to the hypopharynx. It can manifest as issues with chewing, forming a cohesive food bolus, and moving it effectively to the back of the throat.
 * Esophageal dysphagia, on the other hand, is associated with challenges in the passage of food through the esophagus, often causing sensations of food "getting stuck" in the chest.

Physiology of Swallowing
Swallowing is a highly coordinated process that comprises several distinct phases. Here, we delve into the physiological intricacies of this vital function:

 * Swallowing initiates with a voluntary phase in the mouth. During this stage, food is thoroughly masticated (chewed) and mixed with saliva.
 * Following the oral phase, the transfer phase begins as the tongue propels the formed food bolus into the pharynx.
 * Entry into the hypopharynx triggers the pharyngeal swallow response, a centrally mediated sequence of actions aimed at propelling food through the pharynx into the esophagus while guarding against entry into the airway.
 * This process involves the elevation and forward movement of the larynx, facilitating the opening of the upper esophageal sphincter (UES). The bolus is then propelled through the UES by tongue movement and followed by a peristaltic contraction that clears residue from the pharynx and moves it through the esophagus.
 * The lower esophageal sphincter (LES) relaxes to allow the bolus into the stomach.

Musculature and Innervation
Understanding the musculature and innervation of the swallowing process is crucial:

 * The muscles involved in swallowing are striated and directly innervated by lower motor neurons carried in cranial nerves.
 * Specific cranial nerves control different parts of the process, such as the fifth (trigeminal) and seventh (facial) cranial nerves for oral cavity muscles, and the twelfth (hypoglossal) cranial nerve for the tongue.
 * The upper esophageal sphincter (UES) consists of the cricopharyngeus muscle, the adjacent inferior pharyngeal constrictor, and the proximal portion of the cervical esophagus. Its innervation is derived from the vagus nerve.
 * The UES remains closed at rest due to its elastic properties and neurogenically mediated contraction of the cricopharyngeus muscle. It opens during swallowing through a complex coordination of muscle relaxation and movement.

Pathophysiology of Dysphagia
Dysphagia isn't a singular condition; it can be subdivided based on location and underlying causes:

 * Structural dysphagia often results from an oversized bolus or a narrow lumen in the esophagus, causing difficulty in food passage.
 * Propulsive or motor dysphagia arises from abnormalities of peristalsis or impaired sphincter relaxation after swallowing.
 * It's possible for more than one mechanism to contribute to dysphagia in a patient.

Oropharyngeal Dysphagia Causes
Oropharyngeal dysphagia can be attributed to various factors, including:

 * Neurologic causes, such as cerebrovascular accidents, Parkinson's disease, and amyotrophic lateral sclerosis, which affect the neural control of swallowing.
 * Structural issues like Zenker's diverticulum, cricopharyngeal bar, and neoplasia, which hinder the smooth passage of food.
 * Iatrogenic causes, often related to surgeries and radiation treatments in the context of head and neck cancer.
 * Infectious sources, where mucosal ulceration results in painful swallowing (odynophagia).
 * Psychogenic factors like phagophobia (fear of swallowing) or refusal to swallow.

Esophageal Dysphagia Causes
Esophageal dysphagia, primarily centered around the esophagus, has its own set of causes:

 * Structural issues, including Schatzki's rings, eosinophilic esophagitis, and peptic strictures, can narrow the esophageal lumen, making swallowing challenging.
 * Gastroesophageal reflux disease (GERD) can lead to esophageal dysphagia by altering esophageal sensation or motility.
 * Propulsive disorders, such as achalasia, diffuse esophageal spasm, and scleroderma, impact the normal functioning of the esophageal muscles.
 * Various factors, including prior surgery, radiation therapy, and congenital abnormalities, can also contribute to esophageal dysphagia.

Approach to Diagnosis
When dealing with dysphagia, an accurate diagnosis is pivotal. Here's an overview of the diagnostic approach:

 * The patient's history plays a crucial role, helping identify the localization of dysphagia, associated symptoms, and its progression. It can also reveal potential causes, such as prior surgeries or medical conditions.
 * Physical examination can provide insights, especially for oropharyngeal dysphagia, by detecting signs like neuromuscular deficits or inflammatory lesions in the mouth and pharynx.
 * Diagnostic procedures like fluoroscopic swallow studies, otolaryngoscopic evaluations, and endoscopy are employed based on the suspected type and location of dysphagia.

Diagnostic Procedures
In-depth diagnostic procedures are essential in uncovering the underlying causes of dysphagia:

 * Fluoroscopic swallow studies are instrumental in assessing oropharyngeal dysphagia, revealing issues like bolus retention, regurgitation, and aspiration.
 * Upper endoscopy, the primary test for esophageal dysphagia, allows for visualizing mucosal lesions and obtaining biopsies when necessary.
 * Esophageal manometry can confirm esophageal motor disorders, while barium radiography complements the evaluation, especially in complex cases.

Treatment
Effective treatment of dysphagia depends on its specific causes and location:

 * Oropharyngeal dysphagia often benefits from therapy to improve swallowing postures and maneuvers. Altering food consistency can reduce aspiration risk.
 * Esophageal dysphagia may require esophageal dilation for structural issues or surgical interventions for conditions like achalasia or cancer.
 * Infectious etiologies can be treated with antimicrobial medications or management of underlying immunosuppressive conditions.
 * Eosinophilic esophagitis can be addressed through dietary changes, proton pump inhibitors, topical glucocorticoids, and esophageal dilation.

title: Internal Medicine/Dysphagia


text: Category:Book:Wikijunior:Zoo Animal Alphabet


text:
Talk:Public Digital Backbone/4. What is served on my plate? Benefits of Public Digital Backbone

Not able to make pdf of this page
I made a pdf page. Then went back and made a correction, a para break at one place. Then published it and tried to make a pdf. But it is not happening I don't know why. Please guide. Anil Shaligram (discuss • contribs) 14:04, 2 September 2023 (UTC)