Pulmonary vascular disease is defined as a condition of blood
flow to the lung’s artery is blocked suddenly due to a blood clot
somewhere in the body, including pulmonary embolism, chronic
thromboembolic disease, pulmonary arterial hypertension, pulmonary
veno-occlusive disease, pulmonary arteriovenous malformations, pulmonary
edema, etc.
Pulmonary edema
Pulmonary edema is defined as a condition of fluid accumulation in the air spaces and parenchyma of the lungs of that can lead to difficult of breathing and respiratory failure.
I. Signs and Symptoms
Acute pulmonary edema can be classified as either cardiogenic or noncardiogenic or both. Cardiogenic pulmonary edema occurs when the pulmonary capillary hydrostatic pressure exceeds plasma oncotic pressure. Noncardiogenic pulmonary edema occurs when pulmonary capillary permeability is increased(a).
1. Shortness of breath, crepitations, high systolic blood pressure, and chest pain
In the study to
1) describe the prehospital clinical presentation and management of patients with a clinical diagnosis of APE and
2) compare the accuracy of coding of APE by paramedics against the emergency department (ED) medical discharge diagnosis, including a retrospective cohort of all patients who had episodes identified as APE by ambulance paramedics and were transported to a metropolitan hospital ED in 2011, found that four hundred ninety-five patients were transported to an ED with APE identified by the paramedics as the primary problem code. Shortness of breath, crepitations, high systolic blood pressure, and chest pain were the most common presenting signs and symptoms. Pink frothy sputum was rare (3% of patient episodes of APE)(1).
2. Severe respiratory distress with evident inability to adequately ventilate and/or oxygenate
According to the study by the University Hospital of Pisa there is a series of study with the use of intravenous atenolol, a short-acting cardioselective beta-adrenergic antagonist, to treat acute pulmonary edema in the prehospital setting. Four patients with a documented history of cardiac disease and one patient with unknown cardiac issues experienced severe respiratory distress and presented with pulmonary edema; the local emergency medical service was utilized. In all of the patients, the saturation of peripheral oxygen (SpO2) was severely low, and the patients were rapidly treated with oxygen, diuretics, morphine, and nitrates(2).
3. According to the article by Jack Hirsh, MD; John Hoak, MD, patients who survive an acute PE are at high risk for recurrent PE and for the development of pulmonary hypertension and chronic cor pulmonale, which occurs in up to 70% of patients and carries its own attendant mortality and morbidity. Massive PE causes hypotension due to acute cor pulmonale, but the physical examination findings early in submassive PE may be completely normal. Initially, abnormal physical findings are absent in most patients with PE. After 24-72 hours, loss of pulmonary surfactant often causes atelectasis and alveolar infiltrates that are indistinguishable from pneumonia on clinical examination and by x-ray. New wheezing may be appreciated. If pleural lung surfaces are affected, a pulmonary rub may be heard.
The spontaneous onset of chest wall tenderness without a good history of trauma is always worrisome, because patients with PE may have chest wall tenderness as the only physical finding.
In patients with massive PE, the incidence of physical signs has been reported as follows:
96% have tachypnea (respiratory rate >16/min)
58% develop rales 53% have an accentuated second heart sound 44% have tachycardia (heart rate >100/min)
43% have fever (temperature >37.8° C)
36% have diaphoresis
34% have an S3 or S4 gallop
32% have clinical signs and symptoms suggesting thrombophlebitis
24% have lower extremity edema
23% have a cardiac murmur
19% have cyanosis (3)
Chinese Secrets To Fatty Liver And Obesity Reversal
Use The Revolutionary Findings To Achieve
Optimal Health And Loose Weight
Back to General health http://kylejnorton.blogspot.ca/p/general-health.html
Back to Kyle J. Norton Home page http://kylejnorton.blogspot.ca Sources
(a) http://www.ncbi.nlm.nih.gov/pubmed/19739476
(1) http://www.ncbi.nlm.nih.gov/pubmed/23484502
(2) http://www.ncbi.nlm.nih.gov/pubmed/23607890
(3) http://www.mac-paper.com/WebSiteFiles/Miscellaneous/PE.html#Anchor-Authored%20by%20Cr-42694
Pulmonary edema
Pulmonary edema is defined as a condition of fluid accumulation in the air spaces and parenchyma of the lungs of that can lead to difficult of breathing and respiratory failure.
I. Signs and Symptoms
Acute pulmonary edema can be classified as either cardiogenic or noncardiogenic or both. Cardiogenic pulmonary edema occurs when the pulmonary capillary hydrostatic pressure exceeds plasma oncotic pressure. Noncardiogenic pulmonary edema occurs when pulmonary capillary permeability is increased(a).
1. Shortness of breath, crepitations, high systolic blood pressure, and chest pain
In the study to
1) describe the prehospital clinical presentation and management of patients with a clinical diagnosis of APE and
2) compare the accuracy of coding of APE by paramedics against the emergency department (ED) medical discharge diagnosis, including a retrospective cohort of all patients who had episodes identified as APE by ambulance paramedics and were transported to a metropolitan hospital ED in 2011, found that four hundred ninety-five patients were transported to an ED with APE identified by the paramedics as the primary problem code. Shortness of breath, crepitations, high systolic blood pressure, and chest pain were the most common presenting signs and symptoms. Pink frothy sputum was rare (3% of patient episodes of APE)(1).
2. Severe respiratory distress with evident inability to adequately ventilate and/or oxygenate
According to the study by the University Hospital of Pisa there is a series of study with the use of intravenous atenolol, a short-acting cardioselective beta-adrenergic antagonist, to treat acute pulmonary edema in the prehospital setting. Four patients with a documented history of cardiac disease and one patient with unknown cardiac issues experienced severe respiratory distress and presented with pulmonary edema; the local emergency medical service was utilized. In all of the patients, the saturation of peripheral oxygen (SpO2) was severely low, and the patients were rapidly treated with oxygen, diuretics, morphine, and nitrates(2).
3. According to the article by Jack Hirsh, MD; John Hoak, MD, patients who survive an acute PE are at high risk for recurrent PE and for the development of pulmonary hypertension and chronic cor pulmonale, which occurs in up to 70% of patients and carries its own attendant mortality and morbidity. Massive PE causes hypotension due to acute cor pulmonale, but the physical examination findings early in submassive PE may be completely normal. Initially, abnormal physical findings are absent in most patients with PE. After 24-72 hours, loss of pulmonary surfactant often causes atelectasis and alveolar infiltrates that are indistinguishable from pneumonia on clinical examination and by x-ray. New wheezing may be appreciated. If pleural lung surfaces are affected, a pulmonary rub may be heard.
The spontaneous onset of chest wall tenderness without a good history of trauma is always worrisome, because patients with PE may have chest wall tenderness as the only physical finding.
In patients with massive PE, the incidence of physical signs has been reported as follows:
96% have tachypnea (respiratory rate >16/min)
58% develop rales 53% have an accentuated second heart sound 44% have tachycardia (heart rate >100/min)
43% have fever (temperature >37.8° C)
36% have diaphoresis
34% have an S3 or S4 gallop
32% have clinical signs and symptoms suggesting thrombophlebitis
24% have lower extremity edema
23% have a cardiac murmur
19% have cyanosis (3)
Chinese Secrets To Fatty Liver And Obesity Reversal
Use The Revolutionary Findings To Achieve
Optimal Health And Loose Weight
Back to General health http://kylejnorton.blogspot.ca/p/general-health.html
Back to Kyle J. Norton Home page http://kylejnorton.blogspot.ca Sources
(a) http://www.ncbi.nlm.nih.gov/pubmed/19739476
(1) http://www.ncbi.nlm.nih.gov/pubmed/23484502
(2) http://www.ncbi.nlm.nih.gov/pubmed/23607890
(3) http://www.mac-paper.com/WebSiteFiles/Miscellaneous/PE.html#Anchor-Authored%20by%20Cr-42694
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