Dyspnea Symptoms And Causes Quiz! Trivia

ARDS Treatment:
Lung protective ventilation  LOW TIDAL VOLUME VENTILATION
◦ Normal tidal volume 10 ml/kg
◦ Reduce to 8-6 ml/kg
◦ Increase respirator rate to meet minute ventilation

The correct answer is asphyxia and aspiration pneumonia by regurgitation of diverticular contents. In a pharyngeal diverticulum, there is an outpouching of the pharyngeal mucosa, which can collect food and saliva. If the diverticulum becomes large enough, it can cause difficulty swallowing (dysphagia) and lead to the regurgitation of its contents. This can result in asphyxia (difficulty breathing) and aspiration pneumonia (infection of the lungs caused by inhaling foreign material). Therefore, asphyxia and aspiration pneumonia are the dreaded complications of a pharyngeal diverticulum in a 79-year-old lady.

The patient's presentation is consistent with tension pneumothorax, which is a life-threatening condition that requires immediate intervention. The prominent neck veins, tracheal shift, absent breath sounds, and hyper resonance on percussion are all indicative of a tension pneumothorax. The management of choice for tension pneumothorax is to relieve the pressure by inserting multiple wide bore needles into the affected side of the chest to allow air to escape, followed by the insertion of a chest tube to re-expand the lung and prevent recurrence. This intervention should be performed urgently to stabilize the patient's condition.

The histopathologic findings of hyaline membranes and interstitial inflammation are characteristic of viral pneumonia. Hyaline membranes are formed by the accumulation of proteinaceous material in the alveolar spaces, indicating damage to the lining of the lungs. Interstitial inflammation refers to inflammation in the interstitial spaces between the alveoli. These findings are consistent with the patient's symptoms of cough and shortness of breath, as well as the diagnosis of severe viral pneumonia.

A silent chest is the most ominous sign in a patient with an acute asthma attack. This means that there is no audible air movement in the chest, indicating severe airway obstruction. It suggests that the patient's condition is deteriorating rapidly and immediate intervention is required.

Epiglottitis:
 This also presents in childhood but usually in the older child 3 to 4-years-old. It is bacterial associated symptoms include fever, stridor and drooling from the mouth. The epiglottis is swollen and “cherry-red”. Radiologic evidence is the “thumbs up sign” on lateral neck X-Ray. Do not attempt to visualize the epiglottis unless you are able to intubate, as they may go into spasm. Treatment is antibiotics.
Signs and symptoms
Epiglottitis commonly affects children, and it is associated with fever, difficulty in swallowing, drooling, hoarseness of voice, and typically no stridor. The child often appears acutely ill, anxious, and has very quiet shallow breathing with the head held forward, insisting on sitting up in bed. The early symptoms are insidious but rapidly progressive, and swelling of the throat may lead to cyanosis and asphyxiation.
Epiglottitis is an airway emergency and intubation is required initially. ***Since the introduction of the Hemophilus influenzae (Hib) vaccination**** in many Western countries, childhood incidence has decreased while adult incidence has remained the same; the disease is thus becoming relatively more common in adults than children. Modern cases in adults are most typically seen among abusers of crack cocaine, and have a subacute presentation. GEORGE WASHINGTON is one historical figure thought to have died of epiglottitis.

Cause
Epiglottitis involves bacterial infection of the epiglottis, most often caused by Haemophilus influenzae type B, although some cases are attributable to Streptococcus pneumoniae, Streptococcus agalactiae, Staphylococcus aureus, Streptococcus pyogenes, and Moraxella catarrhalis.

The principal result of the increased amount of dissolved CO2 is acidosis (respiratory acidosis when caused by impaired lung function); other effects include tachycardia (rapid heart rate) seizures, coma, respiratory arrest and death.
CO2 retention is a problem in various respiratory diseases, particularly chronic obstructive pulmonary disease (COPD). Patients with COPD who receive excessive supplemental oxygen can develop CO2 retention, and subsequent hypercapnia. The mechanism that underlies this state is a matter of controversy. Some authorities point to a reduction in the hypoxic "drive", a condition called carbon dioxide narcosis. When carbon dioxide levels are chronically elevated, the respiratory center becomes less sensitive to CO2 as a stimulant of the respiratory drive, and the PaO2 provides the primary stimulus for respirations. Administering excess supplemental oxygen can potentially suppress the respiratory center. However, it is unclear whether such a hypoxic drive exists in the first place. An alternative explanation is that, in patients with COPD, the administration of oxygen leads to an increase in the degree to which diseased alveoli are perfused with blood relative to other, less-diseased alveoli. As a result, a larger fraction of blood passes through parts of the lung that are poorly-ventilated, with a resulting increase in the CO2 concentration of the blood leaving the lungs.
As CO2 levels increase, patients exhibit a reduction in overall level of consciousness as well as respiratory effort. Severe increases in CO2 levels can lead to respiratory arrest.
CO2 retention is the hallmark of type II respiratory failure. While in type I any degree of hypoxia is compensated for by hyperventilation (and a decrease in CO2), this mechanism fails in type II. Mechanical ventilation (through intubation, CPAP or BIPAP) may be indicated, or infusion of doxapram.

Cyanosis is divided in to two main types: central (around the core and lips) and peripheral (only the extremities are affected). Cyanosis can occur in the fingers, including underneath the fingernails, as well as other extremities (called peripheral cyanosis), or in the lips and tongue (central cyanosis).
CENTRAL CYANOSIS
Central cyanosis is often due to a circulatory or ventilatory problem that leads to poor blood oxygenation in the lungs. It develops when arterial saturation of blood with oxygen is ≤85%. Cyanosis may not be detected until saturation is 75% in dark-skinned individuals.
Acute cyanosis can be a result of asphyxiation or choking, and is one of the surest signs that respiration is being blocked.
Causes
1. Central Nervous System:
• Intracranial hemorrhage
• Cerebral anoxia
• Drug overdose (e.g. Heroin)
• Tonic-clonic seizure (e.g. grand mal seizure or gran mal seizure)
2. Respiratory System:
• Bronchiolitis
• Bronchospasm (e.g. Asthma)
• Lung disease
• Pulmonary Hypertension
• Pulmonary embolism
• Hypoventilation
• COPD (emphysema and chronic bronchitis)
• Respiratory syncytial virus
3. Cardiac Disorders:
• Congenital heart disease (e.g. Tetralogy of Fallot, Right to left shunts in heart or great vessels)
• Heart failure
• Heart valve disease
• Myocardial infarction
4. Blood:
• Methemoglobinemia
• Polycythaemia
5. Others:
• High altitude
• Hypothermia
• Congenital cyanosis (HbM Boston) arises from a mutation in the α-codon which results in a change of primary sequence, H → Y. Tyrosine stabilises the Fe(III) form (oxyhaemoglobin) creating a permanent T-state of Hb.
• Obstructive sleep apnea

A patient complaining of labored breathing is likely to have dyspnea. Dyspnea refers to difficulty or discomfort in breathing, which can manifest as labored breathing. This symptom may be caused by various underlying conditions such as respiratory infections, asthma, heart failure, or pulmonary embolism. It is important to assess the patient further to determine the cause and provide appropriate treatment.

The most likely finding during the respiratory examination of the attorney would be tachypnea, which refers to rapid breathing. This is because the sudden shortness of breath he experiences is indicative of a respiratory issue. Tachypnea is commonly seen in conditions such as pulmonary embolism, which could be a potential complication following a fracture. Therefore, it is the most likely finding in this scenario.

The acute chest syndrome is a noninfectious vaso-occlusive crisis of the pulmonary vasculature commonly seen in patients with SICKLE CELL ANEMIA. It is characterized by a new infiltrate on a chest x-ray. • Cause The crisis is often initiated by a lung infection, and the resulting inflammation and loss of oxygen tension leads to sickling of red cells and further vasoocclusion. Symptoms The crisis is a common complication in sickle-cell patients and can be associated with one or more symptoms including fever, cough, sputum production, dyspnea, or hypoxia. Treatment Broad spectrum antibiotics to cover common infections like strep pneumoniae and mycoplasma, pain control, and blood transfusion. Prognosis It may result in death, and it is one of the most common causes of death for sickle cell patients.

CYSTIC FIBROSIS is an autosomal recessive genetic disorder affecting most critically the LUNGS, and also the pancreas, liver, and INTESTINE. It is characterized by abnormal transport of chloride and sodium across an epithelium, leading to thick, viscous secretions Gastrointestinal Prior to prenatal and newborn screening, cystic fibrosis was often diagnosed when a newborn infant failed to pass feces (meconium). Meconium may completely block the intestines and cause serious illness. This condition, called meconium ileus, occurs in 5–10%[16][22] of newborns with CF. In addition, protrusion of internal rectal membranes (rectal prolapse) is more common, occurring in as many as 10% of children with CF,[16] and it is caused by increased fecal volume, malnutrition, and increased intra–abdominal pressure due to coughing The lack of digestive enzymes leads to difficulty absorbing nutrients with their subsequent excretion in the feces, a disorder known as malabsorption. Individuals with CF also have difficulties absorbing the fat-soluble vitamins A, D, E, and K. LUNG DISEASE results from clogging of the airways due to mucus build-up, decreased mucociliary clearance, and resulting inflammation. Inflammation and infection cause injury and structural changes to the lungs, leading to a variety of symptoms. In the early stages, incessant coughing, copious phlegm production, and decreased ability to exercise are common. Many of these symptoms occur when bacteria that normally inhabit the thick mucus grow out of control and cause pneumonia. In later stages, changes in the architecture of the lung, such as pathology in the major airways (****BRONCHIECTASIS*****) further exacerbate difficulties in breathing. Summary, Decreased fat digestion, leads to fatty stools. Increased lung infection/inflamation leads to BRONCHIECTASIS

Crackles, crepitations, or rales are the clicking, rattling, or crackling noises that may be made by one or both lungs of a human with a respiratory disease during inhalation Crackles that clear after a cough may indicate pulmonary edema or fluid in the alveoli due to heart failure or Acute Respiratory Distress Syndrome. 1. Crackles are caused by the "popping open" of small airways and alveoli collapsed by fluid, exudate, or lack of aeration during expiration. The word "rales" derives from the French word râle meaning "rattle". 2. Another explanation for crackles is that air bubbles through secretions or incompletely closed airways during EXPIRATION. - ARDS - asthma - bronchiectasis - chronic bronchitis - consolidation - early CHF - interstitial lung disease - pulmonary edema

ARDS Pathophysiology:
Anything that can provoke inflammation to the alveoli can cause it. The lungs are particularly susceptible to inflmamatory mediators generated else where in the body as the entire cardiac output goes through the lungs. Thus a distant inflammatory conditions such as severe pancreatitis can trigger ards. These disease state release inflammatory mediators that produce diffuse alveolar damage

Diaphragmatic hernia is characterized by tympany on chest percussion. Tympany refers to a drum-like sound that is produced when a hollow organ, such as the stomach or intestines, is percussed. In diaphragmatic hernia, a portion of the abdominal organs protrudes through an opening in the diaphragm into the chest cavity. This can lead to air accumulation in the chest, causing the characteristic tympany sound on percussion. Bronchial asthma, lung emphysema, and pulmonary embolism do not typically result in tympany on chest percussion.

Based on the given information, the patient presents with acute onset of shortness of breath (SOB) and a low oxygen saturation level of 84%. This indicates that the patient is experiencing hypercapnic respiratory failure, which is characterized by an elevated level of carbon dioxide (hypercapnia) in the blood. Hypercapnic respiratory failure occurs when there is inadequate ventilation or impaired gas exchange, leading to an accumulation of carbon dioxide and a decrease in oxygen levels.