Disorders Of The Respiratory System Memo

Disorders Of The Respiratory System Memo

Disorders Of The Respiratory System Memo

The Most Common Signs and Symptoms of Respiratory Insufficiency
On clinical examination, respiratory disease manifests itself as one or more of number of indications. 
The symptoms differ depending on the disease’s cause and anatomic location. 
Hypoxemia and hypercapnia are life-threatening disorders in diseases that limit breathing or gas exchange. 
As result of systemic inflammatory response and toxemia, infectious and inflammatory illnesses can induce significant clinical abnormalities. 
Even if oxygen and carbon dioxide exchange are not considerably hindered, the toxemia can be severe enough to cause death (e.g., in calf diphtheria, aspiration pneumonia, and equine pleuritis). 
The following are some of the most prevalent symptoms of respiratory disease:
• Coughing • Cyanosis • Nasal discharge • Epistaxis and hemoptysis • Lethargy or activity intolerance • Abnormal posture • Abnormal lung sounds • Abnormal respiratory noises • Coughing • Cyanosis • Nasal discharge
Breathing Rate, Depth, and Ease Abnormalities
Polypnea is characterized by higher rate of breathing than that seen in clinically normal animals of the same species, breed, age, sex, and reproductive state in the same environment.


Tachypnea also indicates an accelerated rate of breathing, however with the suggestion that breathing is shallow (i.e., of lower tidal volume) (i.e., of reduced tidal volume).
Hyperpnea is characterized by an abnormal increase in the rate and depth of breathing (an unusually high minute volume), but the breathing is not laborious and is not accompanied by any symptoms that indicate the animal is in discomfort (i.e., the animal is not dyspneic). 
Minute ventilation or arterial blood gas tensions must be measured for this assessment.


Dyspnea is term adopted from human medicine to describe feeling of shortness of breath or lack of oxygen. 
It’s term used in veterinary medicine to describe hard or difficult breathing in animals with other indicators of discomfort, such as an anxious countenance, aberrant posture or stance, or strange behavior.

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Dyspnea is normal physiologic reaction to strenuous exercise, and it is only abnormal when it occurs at rest or with little exercise. 
Hypoxia with or without hypercapnia is the most prevalent cause, and it is most commonly caused by respiratory tract illnesses. 
Another factor that may play role in pulmonary dyspnea is an excessively sensitive Hering–Breuer reflex. 
This is most likely to happen when the lungs or pleura are inflamed or congested. 
As result, rapid, shallow breathing occurs.
Expiratory dyspnea is symptom of obstructive lower airway illness that is characterized by prolonged and forceful expiration. It is most commonly associated with diffuse or advanced obstructive lower airway disease. 
The dyspnea associated with pulmonary emphysema is often expiratory in nature, and is produced by anoxic anoxia and the necessity for forceful expiration to achieve successful tidal air ejection. 
In ruminants, it is frequently accompanied by an audible expiratory grunt, but not in pigs and virtually never in horses.


The obstruction of the extrathoracic airways, such as laryngeal obstruction or collapse of the cervical trachea, causes inspiratory dyspnea, which is defined as prolonged and forceful inspiration. 
It may also be linked to thoracic anomalies that limit expansion, such as restrictive lung disorders and thoracic space-occupying lesions. 
When the reason is obstruction of the extrathoracic airways, such as is typical of laryngeal or tracheal illness, it is accompanied with stridor or loud sharp sound on inspiration.


Open-mouth breathing is labored breathing with the mouth open, often with the tongue protruding in ruminants, and is most often linked with severe pulmonary disease or nasal blockage.

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Dyspnea at rest or lack of exercise tolerance are both diseases that cause dyspnea.


The clinical and laboratory symptoms most likely to draw attention to the presence of disease in the respiratory system include dyspnea, hypoxemia, and hypercapnia. 
When seeking to distinguish disorders that cause dyspnea, it is critical to consider diseases that affect systems other than the respiratory system. 
Exercise intolerance can be caused by disease in the respiratory, cardiovascular, musculoskeletal, or other body systems, whereas dyspnea at rest is frequently but not always caused by respiratory tract disease.


Diseases of the Respiratory Tract


Through the mechanisms outlined above, respiratory tract illnesses obstruct proper gas transfer. 
The following are characteristics of respiratory disease that cause dyspnea or lack of exercise tolerance:
• Inflammatory cells and/or protein-rich fluid flooding the alveoli—pneumonia and pulmonary edema
Pleural effusion, hemothorax, hydrothorax, pneumothorax, chylothorax, pyothorax, prolonged recumbency of large animals, and diaphragmatic hernia are all examples of atelectasis (collapsed alveoli and small airways).
• Nasal obstruction, pharyngeal/laryngeal obstruction, tracheal/bronchial obstruction, bronchoconstriction, and bronchiolar obstruction are all examples of airway obstruction.


Diseases of the Cardiovascular System


Inadequate perfusion of tissues, including the lungs, is result of cardiovascular disease. 
Even when arterial oxygenation is normal, there is reduction in oxygen delivery to tissues.


Cardiac disease is condition that affects the heart. 
Cardiac dyspnea is multifactorial condition that occurs as result of heart failure. 
There are other obvious signs of heart failure in animals with dyspnea caused by cardiac disease.


• Peripheral circulatory failure—usually due to hypovolemic shock, but toxemia-related shock, such as endotoxemia, can also produce dyspnea. 
Other obvious indications of sickness are always present.


Blood-related illnesses


Because of anemia or the existence of hemoglobin that is unable to carry oxygen, diseases of the blood cause insufficient oxygen delivery to tissues.


• Anemia (abnormally low hemoglobin concentration)

Disorders Of The Respiratory System Memo

• Methemoglobinemia (e.g., nitrite poisoning in cattle, red maple toxicosis in horses), Carboxyhemoglobinemia (e.g., nitrite poisoning in cattle, red maple toxicosis in horses).

Case Study Analysis

A 38-year-old female with a history of systemic lupus erythematosus and on oral contraceptives presents with dyspnea and left leg pain. The patient reports erythema on her left leg and denies injury to her leg. Her BP is 130/84, HR is 100, R is 24, and temperature is 100.4F. Physical exam reveals unilateral +2 pitting leg edema at the left leg with erythema. The purpose of the paper is to describe the pulmonary pathophysiologic processes, any racial variables that impact physiologic functioning, and how the processes interact to affect the patient.

The Pulmonary Pathophysiologic Processes That Result In These Symptoms

The patient presents with an acute episode of pulmonary embolism (PE) secondary to deep venous thrombosis (DVT). Virchow’s triad, which includes venous stasis, endothelial injury, and hypercoagulability, contributes to the formation of a thrombus (Navarette et al., 2023). The patient has all the risk factors for DVT development, including systemic lupus erythematosus causing endothelial damage, venous stasis due to long air travel, and hypercoagulability associated with oral contraceptives. PE occurs when the deep venous thrombi detach and embolize to the pulmonary circulation, leading to pulmonary vascular occlusion and impaired gas exchange and circulation (Shah et al., 2022). As a result, dead space ventilation and hypoxemia occur due to obstruction of the pulmonary arteries and reduced capillary blood flow. Hyperventilation due to hypoxemia occurs despite obstructed blood flow, resulting in dyspnea and secondary respiratory acidosis.

Racial Or Ethnic Variables That May Impact Physiological Functioning

The most common risk factors that predispose persons to develop DVT include genetic mutations in anticoagulant proteins such as factor V Leiden and the prothrombin gene. In addition, deficiencies in anti-thrombin, protein C, and protein S contribute to DVT. The mutations are more common in Caucasians than in Black Americans (Farmakis et al., 2023). However, despite the prevalence of such mutations in Caucasians, Black Americans have a higher risk of developing DVT and its complications.

How These Processes Interact to Affect the Patient…

Obstruction in pulmonary blood flow increases pulmonary vascular resistance and right ventricular afterload. As a result, there is an obstruction in right ventricular outflow, resulting in dilatation of the ventricle and right-sided heart failure, which increases patient mortality (Freund et al., 2022). In addition, there is a reduction in inflow to the left ventricle, resulting in reduced cardiac output. Systemic hypotension and hemodynamic instability with resultant tissue hypoxia occur as a result of reduced cardiac output, worsening the prognosis. Long-standing pulmonary embolism has also been associated with the formation of multiple lung infarcts.


DVT and PE have a higher risk of developing when one or all the components of Virchow’s triad are involved. Dyspnea due to PE occurs as a result of obstructed blood flow to well-ventilated areas of the lung. Mortality due to PE has been associated due to the hemodynamic instability it causes in the patient’s circulation.


Farmakis, I. T., Valerio, L., Giannakoulas, G., Hobohm, L., Cushman, M., Piazza, G., Konstantinides, S. V., & Barco, S. (2023). Social determinants of health in pulmonary embolism management and outcome in hospitals: Insights from the United States nationwide inpatient sample. Research and practice in thrombosis and haemostasis, 7(3), 100147.

Freund, Y., Cohen-Aubart, F., & Bloom, B. (2022). Acute Pulmonary Embolism: A Review. JAMA, 328(13), 1336–1345.

Navarrete, S., Solar, C., Tapia, R., Pereira, J., Fuentes, E., & Palomo, I. (2023). Pathophysiology of deep vein thrombosis. Clinical and experimental medicine, 23(3), 645–654.

Shah, I. K., Merfeld, J. M., Chun, J., & Tak, T. (2022). Pathophysiology and Management of Pulmonary Embolism. The International journal of angiology : official publication of the International College of Angiology, Inc, 31(3), 143–149.