3871552
Beschreibung
Karteikarten von tiwariashley, aktualisiert more than 1 year ago
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Erstellt von tiwariashley
vor etwa 9 Jahre
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| Frage | Antworten |
| Where is lead 1 located | between right arm and left arm; the left arm is positive |
| where is lead 2 located | between the right arm and left leg; left leg is positive |
| where is lead 3 located | between the left arm and left leg; left leg being positive |
| ECG leads | they detect a change in electric potential between two points) and detect the electrical potential change in the frontal plane. |
| V1 location | Fourth intercostal space to the right of the sternum. |
| V2 location | Fourth intercostal space to the Left of the sternum. |
| V3 location | between V2 and V4; between fourth and fifth intercostal space |
| V4 location | Fifth intercostal space at midclavicular line |
| V5 | Level with V4 at left anterior axillary line |
| V6 | Level with V5 at left midaxillary line; Directly under the midpoint of the armpit |
| V1 and V2 detect | right ventricle |
| V3 and V4 | Septum/ lateral left ventricle |
| V5 and V6 | Anterior/lateral left ventricle |
| myocardial infarction | The blood supply to certain areas of the myocardium is obstructed. The muscle tissue at the center of the infarct dies off |
| Cause of Myocardial infarction associated with atherosclerosis | plaque builds up in the walls of your coronary arteries. This plaque is made up of cholesterol and other cells |
| Other causes for heart attack | Stress Male gender Diabetes Family history of coronary artery disease (genetic or hereditary factors) High blood pressure Smoking Unhealthy cholesterol levels, especially high LDL ("bad") cholesterol and low HDL ("good") cholesterol. Chronic kidney disease |
| Symptoms for Heart attack | chest pain lasting longer than 20 minutes Sweating Anxiety Cough Fainting Dizziness Nausea or vomiting Palpitations (feeling like your heart is beating too fast) Dyspnea |
| Pain from Heart attacks might feel like | A tight band around the chest Bad indigestion Something heavy sitting on your chest Squeezing or heavy pressure |
| How to diagnose myocardial infarction | 1. history of chest pain > 20 min 2. Changes in ECG tracings 3. Rise/ Fall of serum cardiac biomarkers 4. If there is a high positive R, there is also a Larger negative Q waves, ST segment elevation or depression, or coronary intervention are diagnostic of MI. |
| What are the cardiac troponins which are released within 4–6 hours of an attack of MI and how long do they stay elevated for | T and I and remain elevated for up to 2 weeks |
| Management for heart attack | which requires immediate medical attention. Oxygen, aspirin, and nitroglycerin. |
| Endocarditis | inflammation of the inside lining of the heart chambers and heart valves (endocardium |
| Endocarditis is usually a result of | blood infection |
| What are some things that increase chances for developing endocarditis: | Artificial heart valves Congenital heart disease Heart valve problems History of rheumatic heart disease |
| symptoms | Abnormal urine color Chills (common) Excessive sweating (common) Fatigue Fever (common) Joint pain Muscle aches and pains Night sweats Nail abnormalities (splinter hemorrhages under the nails) Paleness |
| How to test for myocarditis | Blood culture and sensitivity (to detect bacteria) Chest x-ray Complete blood count (may show mild anemia) Echocardiogram (ultrasound of the heart) Erythrocyte sedimentation rate (ESR) Transesophageal echocardiogram |
| Treatment for myocarditis | Long-term, high-dose antibiotic treatment is needed to get rid of the bacteria. Treatment is usually given for 4-6 weeks, depending on the specific type of bacteria. Blood tests will help your doctor choose the best antibiotic. Surgery may be needed to replace damage heart valves. |
| Mitral stenosis | heart valve disorder that involves the mitral valve |
| Stenosis | refers to a condition in which the valve does not open fully, restricting blood flow. |
| Causes for mitral stenosis | the valve area becomes smaller, less blood flows to the body. The upper heart chamber swells as pressure builds up. Blood may flow back into the lungs. Fluid then collects in the lung tissue (pulmonary edema), making it hard to breathe. |
| Symptoms for mitral stenosis | Atrial fibrillation -Chest discomfort (rare): Increases with activity, decreases with rest -Radiates to the arm, neck, jaw, or other areas Tight, crushing, pressure, -Cough, possibly bloody (hemoptysis) Difficulty breathing during or after exercise or when lying flat; may wake up with difficulty breathing -Fatigue, becoming tired easily - Bronchitis -Palpitations -Swelling of feet or ankles |
| Complications mitral stenosis | Atrial fibrillation and atrial flutter -Blood clots to the brain (stroke), intestines, kidneys, or other areas -Heart failure -Pulmonary edema -Pulmonary hypertension |
| In the ECG for mitral stenosis | There is atrial fibrillation. No P waves are visible. The rhythm is irregularly irregular (random). With severe pulmonary hypertension, right ventricular hypertrophy can be seen. |
| Treatment for mitral stenosis | Cardiac Glycosides Diuretics -β-blockers -Ca2+ channel blockers -Anticoagulants -balloon valvotomy -surgical commissurotomy -valve replacement Digoxin |
| Negatively chronotropic Digoxin | slowing the heart rate by decreasing conduction of electrical impulses through the AV node, making it a commonly used antiarrhythmic agent in controlling the heart rate during atrial fibrillation or atrial flutter. |
| Positively inotropic digoxin | increasing the force of heart contraction via inhibition of the Na+/K+ ATPase pump. |
| Mitral regurgitation | long-term disorder in which the heart's mitral valve does not close properly, causing blood to flow backward (leak) into the upper heart chamber when the left lower heart chamber contracts. The condition is progressive, which means it gradually gets worse. |
| causes for mitral regurgitation | Mitral valve prolapse -Congenital -Atherosclerosis -Endocarditis -Heart tumors -High blood pressure -Marfan syndrome -Untreated syphilis |
| Symptoms for mitral regurgitation | Cough -Fatigue -Palpitations (related to atrial fibrillation) -Shortness of breath during activity and when lying down -Urination, excessive at night enlarged liver |
| Treatment | Antibiotics reduce the risk of infective endocarditis in patients with mitral valve prolapse who are having dental work. -Antihypertensive drugs and vasodilators. -Anticoagulant or antiplatelet medications prevent clot formation in patients with atrial fibrillation. - Digitalis may be used to strengthen the heartbeat, along with diuretics to remove excess fluid in the lungs. |
| Cerebral cardiac output percentage | 15 percent |
| coronary cardiac output percentage | 5 percent |
| renal cardiac output percentage | 25% |
| Gastrointestinal cardiac output percentage | 25 percent |
| skeletal cardiac output percentage | 25 percent |
| skin cardiac output percentage | 5 percent |
| Regulating of arterial Pressure fast mechanism | neural baroreceptor |
| Regulating of arterial Pressure slow mechanism | hormonal (renin-angiotensin-aldosterone) |
| Baroreceptor reflex is a _______ _______ _______ that is responsible for the minute-to-minute regulation of arterial pressure. | negative feedback system |
| Baroreceptors are stretch receptors located within the walls of the______ _____near the bifurcation of the common carotid arteries. | carotid sinus |
| four effects attempt to increase the arterial pressure to normal | Increases heart rate Increases contractility and stroke volume Increases vasoconstriction of arterioles Increases vasoconstriction of veins |
| Example of the baroreceptor reflex | response to acute blood loss |
| .Renin-angiotensin-aldosterone system | is a slow, hormonal mechanism and Regulation by adjustment of blood volume. |
| -Renin | is an enzyme. |
| Angiotensin I | is inactive. |
| Angiotensin II | is physiologically active and is degraded by angiotensinase. |
| Example : response of the RAA system | acute blood loss |
| Other regulation of arterial blood pressure | Cerebral ischemia Chemoreceptors in the carotid and aortic bodies Vasaopressin (antidiuretic hormone) Atrial natriuretic peptide (ANP |
| Cerebral ischemia | Pco2 pressure increases in brain tissue. b. Chemoreceptors in the vasomotor center respond by increasing sympathetic outflow to the heart and blood vessels. Constriction of arterioles causes intense peripheral vasoconstriction and increased TPR. Blood flow to other organs (kidneys) is significantly reduced in an attempt to preserve blood flow to the brain. |
| The Cushing reaction in an example of the response to | cerebral ischemia |
| Cushing reaction | Increases intracranial pressure cause compression of the cerebral blood vessels, leading to cerebral ischemia and increased cerebral Pco2. The vasomotor center directs an increase in sympathetic outflow to the heart and blood vessels, which causes a profound increase in arterial pressure. |
| Chemoreceptors in the carotid and aortic bodies are located near | the bifurcation of the common carotid arteries and along the aortic arch. |
| Chemoreceptors in the carotid and aortic bodies have very high rates of | O2 consumption and are very sensitive to decreases in the partial pressure of oxygen (Po2). |
| Decreases in Po2 activate vasomotor centers that produce | vasoconstriction, an increase in TPR, and an increase in arterial pressure. |
| Atrial Natriuretic peptide binds to a specific set of receptors. Receptor-agonist binding causes | causes a reduction in blood volume and therefore a reduction in cardiac output and systemic blood pressure. |
| Atrial Natriuretic peptide Inhibits | renin secretion, thereby inhibiting the renin-angiotensin system. |
| Atrial Natriuretic peptide Reduces_______ secretion by the adrenal cortex. | aldosterone |
| Atrial Natriuretic peptide Relaxes vascular smooth muscle in | arterioles and venules. |
| True capillaries do not have | smooth muscle; they consist of a single layer of endothelial cells surrounded by a basement membrane |
| Blood flow through the capillaries is regulated by __________ and _________of the arterioles and the precapillary sphincters. | contraction and relaxation |
| Clefts (pores) between the endothelial cells allow passage | of water-soluble substances. The clefts represent a very small fraction of the surface area |
| At the junction of the arterioles and capillaries is a smooth muscle | band called the precapillary sphincter. |
| Passage of substances across the capillary wall | Lipid-soluble substances (o2 and CO2) . Small water-soluble substance Large water-soluble substances |
| How do small water soluble substance cross the capillary wall | via the water-filled clefts between the endothelial cells. |
| In the liver and intestine, the clefts of the capillary wall are | exceptionally wide and allow passage of protein. These capillaries are called sinusoids. |
| how do large water soluble substances cross across the capillary wall | pinocytosis |
| Function of lymph | , filtration of fluid out of the capillaries is slightly greater than absorption of fluid into the capillaries. The excess filtered fluid is returned to the circulation via the lymph. Lymph also returns any filtered protein to the circulation. |
| Unidirectional flow of lymph | one-way flap valves permit interstitial to enter, but not leave, the lymph vessels. -Flow through larger lymphatic vessels is also unidirectional, and is aided by one-way valves and skeletal muscle contraction. |
| Edema | occurs when the volume of interstitial fluid exceeds the capacity of the lymphatic to return it to the circulation. -can be caused by excess filtration or blocked lymphatics. |
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