pulmonary artery hypertension

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Slide 1 : PULMONARY ARTERIAL HYPERTENSION
Slide 2 : INTRODUCTION WHAT IS PAH? WHAT CAUSES PAH? SIGNS AND SYMPTOMS DIAGNOSIS
Slide 3 : H I S T O R Y The first reported case – 1891 E. Romberg, German doctor published description of a patient who, at autopsy, showed thickening of the pulmonary artery but no heart or lung disease In 1951, 39 cases were reported by Dr. D.T. Dresdale in the United States. The illness received its name. Between 1967 and 1973, a 10-fold increase in unexplained pulmonary hypertension was reported in central Europe. The rise was subsequently traced to aminorex fumarate, an amphetamine-like drug introduced in Europe in 1965 to control appetite. It was later removed from the market.
Slide 4 : INTRODUCTION 500 – 1000 new cases diagnosed annually Incidence : 2-3 per million per year Prevalence :15 per million. Men, Women and Children of all ages Most common in females between 20 and 40 years old, with twice as many cases reported in women then men Rare in children but is sometimes seen in infants born with heart defects. Pulmonary hypertension may be a primary or secondary cause of hypoxia in neonates.
Slide 5 : THE PULMONARY CIRCULATION IS CHARACTERISED BY: HIGH FLOW LOW PRESSURE LOW RESISTANCE PAH ? PRESSURE ? RESISTANCE
Slide 6 : Hence, blood pressure is usually much lower in the lungs. Pulmonary arteries- 24/9 mm Hg General circulation-120/80 mm Hg
Slide 7 : Mean (average) pulmonary artery pressure = diastolic + 1/3 of diff between systolic & diastolic Normal at rest : 14 mm Hg Pulmonary hypertension at rest : 25 mm Hg during exercise : 30 mm Hg
Slide 8 : REGULATION OF PULMONARY VASCULAR TONE AND BLOOD FLOW I> ALVEOLAR OXYGENATION Alveolar hypoxia Local vasoconstriction Chronic hypoxemia causes sustained elevation of pulmonary artery pressure, vascular remodeling mediated by a number of growth factors(vascular endothelial growth factor) and development of PAH.
Slide 9 : II> NITRIC OXIDE Relaxes vascular smooth muscles Endothelial nitric oxide synthase is found in vascular endothelium of normal pulmonary vasculature, where it generates nitric oxide. In addition, it inhibits growth of vascular smooth muscle cells. HENCE, ENDOTHELIAL DUSFUNCTION CONSTRICTION OF VASCULAR SMOOTH MUSCLE CELLS DISINHIBITION OF GROWTH OF VASCULAR SMOOTH MUSCLE CELLS
Slide 10 : Injury to endothelial cells leads to overproduction of endothelin – key cause of blood vessel scarring and spasm & to reduced production of nitric oxide and prostacyclins – 2 key body chemicals which keep blood vessels relaxed and open.
Slide 11 : III>ADRENERGIC CONTROL BETA RECEPTORS: VASODILATION ALPHA RECEPTORS: VASOCONSTRICTION
Slide 12 : WHAT CAUSES PULMONARY HYPERTENSION?
Slide 13 : Primary Pulmonary Hypertension no underlying cause for the high blood pressure in lungs likely to begin with spasm of the muscle layer in pulmonary arteries patients are rather sensitive to substances that cause blood vessels to constrict may have an inherited predisposition for the disease
Slide 14 : Secondary Pulmonary Hypertension Results directly from another medical problem Most probable from diseases that impedes flow of blood through lungs or that causes periods of low oxygen in blood eg. Chronic Obstructive Pulmonary Disease, scleroderma, sleep apnea, pulmonary fibrosis, lung diseases such as asbestosis
Slide 15 : The overall rise in blood pressure in PH is the end result of a process which begins with changes in the endothelial cells that line the lungs’ arteries. Changes ? causes formation of extra tissue ? blockage in vessels Scarring (fibrosis) usually also occurs ? arteries stiff and narrow These causes increased resistance to blood flow which raises pressure in the pulmonary arteries. Less often, PH is caused by extensive loss of lung tissue from surgery/trauma.
Slide 16 : THE ‘TWO-HIT’ HYPOTHESIS According to the hypothesis, vascular abnormalities characteristic of PPH are triggered by accumulation of genetic and/or environmental insults in a susceptible individual. A combination of germline BMPR2 mutation (‘first hit’) and the ingestion of appetite suppressants (‘second hit’) were used to generate the clinical disease.
Slide 17 :
Slide 18 : In some people, the bone marrow will produce more red blood cells to compensate for less of oxygen in blood leading to Polycythemia HYPER VISCOSITY-Extra RBCs cause the blood to become thicker and stickier, further increasing the load on the heart Pulmonary Embolism
Slide 19 : SYMPTOMS AND SIGNS
Slide 20 : Subtle in the early stages of the disease May not be apparent for months or even years As the disease progresses, these signs become more noticeable Also, the symptoms of PH are often hidden by the underlying condition causing the disease. Symptoms, however, tend to vary from patient to patient
Slide 21 : shortness of breath (dyspnea) Initially, only short of breath when exert oneself physically but eventually may be short of breath most of the time, even when at rest.
Slide 22 : fatigue or light-headed upon exertion dizziness or fainting spells (syncope) swelling (edema) in ankles, legs and eventually in abdomen (ascites) – fluid leak out of veins and into tissues bluish colour to lips and skin (cyanosis)
Slide 23 : coughing (sometimes with blood) and wheezing racing pulse or heart palpitations angina-like chest pain feel weak – body tissues not receiving enough oxygen achy joints (often developed years before apparent onset of disorder)
Slide 24 : RAISED JVP PALPABLE P 2 LEFT PARASTERNA HEAVE TRICISPID REGURGITATION MURMUR
Slide 25 : DIAGNOSIS OF PAH
Slide 26 : It is often very difficult to initially diagnose PH. In fact, there is often a lengthy delay between the time when patients first visit their doctor and the time they receive specialist care at a hospital. Since there is no single test that will tell the healthcare team if a patient has PH, it is important to consider all associated diseases as well as other causes of breathlessness, such as certain lung and heart diseases and blood clots. A definite diagnosis of PH usually requires passing a tube through a vein in an arm or a leg into the right side of the heart to measure the blood pressure in the right ventricle and the pulmonary artery
Slide 27 : For patients with suspected PH, there are several initial steps that are commonly taken to confirm the diagnosis. These are first discussed between the patient and the healthcare team : history of present illnesses past medical history family history any past or present medications that the patient may have taken A thorough physical examination will also take place. After this, a number of tests may be ordered to aid in assessment and diagnosis of PH.
Slide 28 : CHEST X-RAY
Slide 29 : Echocardiography (Ultrasonic Cardiography) This test uses sound waves to track the structure and function of the heart. It can compose images of a beating heart on a monitor and detects: heart’s thickness, size and function motion pattern and structure of the four heart valves ? revealing any potential leakage (regurgitation) thickening of right ventricle, enlarged right heart reversal of blood through tricuspid valve extent of lung damage A specific echocardiogram, Doppler ultrasound, is sometimes used to determine pulmonary artery pressure. Exercise echocardiogram – determine how well heart works under stress
Slide 30 :
Slide 31 : Electrocardiogram (ECG)
Slide 32 : Pulmonary Angiogram Used to measure circulation in the lungs and to visualize clots in the lung on x-rays. The test involves insertion of a thin catheter into the pulmonary artery through which an iodine dye is injected. Image of any blood clots present in the lung can be observed and circulation of blood through lung’s blood vessels can be tracked.
Slide 33 : Perfusion Lung Scan Uses small amounts of radioactive tracers (radioisotopes) to study blood flow in the lungs. Radioisotopes are attached to radiopharmaceuticals which are then injected into a vein the arm. A gamma camera takes pictures of blood flow in the lungs’ blood vessels. It is generally used to determine whether blood clots may be causing symptoms of PH.
Slide 34 : Pulmonary Function Tests Non-invasive tests to measure how much air your lungs can hold and the airflow in and out of your lungs. They can also measure the amount of gases exchanged across the membrane between the lung wall and capillary membrane. During the tests, the patient will be asked to blow into a spirometer. An abnormality here may be amongst the first indication of PH.
Slide 35 : CT SCAN MRI OTHER SCREENIG METHODS exercise testing-6 min walk test ventilation-perfusion (V/O) scanning arterial blood gas studies central hematocrit count serum glucose and calcium levels count platelet count hyperoxia (100% oxygen) challenge test
Slide 36 :

 


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