Med-surg Restrictive breathing: can't get enough air in: increased hr, increased resp rate.

shallow, rapid breathers. Tx: fix cause. TB: antibiotics, 4 of them of 6 months min Latent vs active. Latent= PPD is active or has been. 6 months of antibiotics. Correct way to read: run ball point pen till it point of induration stops and measure. Incorrect readings in vaccinated ptnts, immunocompromised ptnts, and prednisone. 10ml or more, 5 ml or more. Quantaferon is serum marker for disease: Gold standard but expensive. Manifestations: Chronic cough, fatigue weight loss due to body burning energy to fight it, fever, coughing up blood, night sweats. Interventions: DOT: Directly observed therapy. Recommended by CDC for all patients Surgery: pneumonectomy, lobectomy, segmetetomy, wedge resection. When this happens, there may be lung sounds there because other lobes are moving over. Pneumonectomy- rise and fall of chest is undequal. Pain, may need o2, will likely have chest tube. Monitor o2, breathsounds, asses incision, suction on chest tube. Air in the pleural space may sound like decreased breath sounds.

Know chest tube~ measure output of blood. With negative pressure is the chest tube working. Discharge instructions. Range of motion exercises for arm.

For pneumonia: anitbiotics. Nursing interventions: make sure they take the whole thing Start IV within 4 hours. H1N1: Tx: tamaflu- antiviral May need fluids or aniemucoliticis Cystic fibrosis: wall is thickiened and air cant get through. Supportive care: o2 and pulse ox. Obstructive:

Asthma is an itis Asthma: inflammation mucousdecreased airflow. Wheezing, chest tightening, SOB.

Chronic. Triggers are individual. Difference is the severity of response to different triggers. If your airways stay inflamed you have long term damage. Bronchiol constriction blocks air from coming back out. Now, if aair cant get out, there is not enough room for new air to get in. Disorder of the immune system. Goals of asthma therapy: datime symptoms, none or less than twice a week. No limitations, no nocturnal symptoms, need for rescue/reliever tx used 0-2x per week, lung function is normal. Asthma management: 4 Awareness, meds, action plan, trigger identification/control. Triggers: Allergens, exercises irritants, foods-sulfites. Sulfites in preserved fruit. Tx: steroids Dust Mites allergies: special sheets, no curtains, carpets Peak Flow meter: measures flow out. Take the best reading out of 3 readings. Restrictive lung disease there is no loss of elasticity. We just have difficulty getting the air in. And there is more tension to push the air out. So peak flow is increased. Obstructive: there is loss of elasticity: Peak flow is decreased. Inhaled steroids for asthma to reduce inflamations respose. Spirometry: For asthmatics, less than a third of the air gets out than in a normal person. After tx with bronchodilator, more air can come out. Normal breath, Normal tidal volume: 500 mls of air in and uot, so half a liter is normal breath. Vital capacity squeeze air out COPD: Includes Emphysema and Chronic Bronchitis Emphysema: Loss of elacticity and hyperinflation of lungsdyspnea and Inc resp rate. Causes: Proteases attack and eliminate particulate in healthy lung. In smokers, there is more and more particulate around and the proteases are present in increased amounts and can do significant damage

to the alveoli, causing them to lose their elasticity, and the small airways tot collapse and narrow. Some alveoli are destroyed and others become large and flabby and are called bullae, (blisters). A significant amount of air is trapped. When this lung is hyperinflated, the diaphragm becomes flattened and cannot work as effectively. As a result, the patient needs accessory muscles to breath effectively. The use of accessory muscles demands an even greater amount of oxygen. This makes the patient work harder, and causes, air hunger. This patient may have an increased respiratory rate to compensate, and arterial blood gasses will be normal until the disease is advanced. When that happens. CO2 is made faster and cannot be eliminated as quickly as it needs to be, then leading to chronic respiratory acidosis. In late stage, the person will also have low PaO2 levels as the blood cannot move effectively into the blood from the diseased alveoli. Three Types of Emphysema: Panlobular, Centilobular, or Paraceptal. Most are associated with smoking or other exposure to irritants. Chronic Bronchitis: Inflammation of the bronchi or bronchioles caused by exposure to irritants, esp cigarettes. The irritant causes inflammation, vasodilation, mucosal edema, congestion and bronchospasm. Difference is, bronchitis affects the bronchioles and not the alveoli. Chronic inflammation--?increased number and size of mucous glands, thus producing large amounts of thick mucous. The bronciol walls thicken and along with the excessive mucous, there is blockage of some of the smaller airways. Also, the increased amounts of mucous are an ideal breeding ground for microorganisms and lead to chronic low-grade infections. As mucous plugs block the airways, PaO2 is blocked from getting in and CO2 blocked from getting out.

Etiology and Risks: Cigarettes. 8 pack year history: Often some obstructive lung damage, but no manifestations of disease 20 pack year history: Early stage COPD with changes in pulmonary function tests. Cause: excessive smoke excessive protease release breakdown of elastin in alveoli. Also, damage to the cilia prevent the bronchi from clearing fluid, mucous, and cellular debris. Secondhand and Thirdhand Smoke, (third is that that clings to hair and clothing). Smoking is highest in northern plains American Indians and Alaskan Natives. Also, African Americans, blue collared workers, and uneducated workers. Alpha1-antitrypsin deficiency, (AAT deficiency), is a protease inhibitor that prevents proteases from working on the lungs. Those with this deficiency are also at risk Complications: Oxygenation of all tissues. Tissue anorexia and death. Hypoxemia, acidosis, respiratory infections, cardiac failures, and dysrhythmias. Common respiratory infections: Streptococcus Pneumoniae, haemophilus influenza, and Moraxella catarrhalis.

Cardiac Failure, esp Cor pulmonale, (right sided heart failure caused by pulmonary disease). The increased pressure in the lungs put increased pressure on the lung vessels, making the right side f the heart work harder trying to pump blood into the lungs. In turn, the right side of the heart enlarges and thickens and there is general back up of blood in the venous system. Cardiac dysrhythmias happen as there is less blood to oxygenate the heart. Labs: Hypoxemia and hypercarbia (inc CO2). Elevated CO3 as kidneys try to compensate for respiratory acidosis. pH is still low (acidic). Hgb and Hct are ordered, and polecythemia is generally seen as a compensatory mechanism for the lack of O2. Sputum Samples and WBC counts. Electrolytes: Low phosphate, potassium, calcium, magnesium reduced muscle strength. Serum AATs with those that have family history of COPD. Chest X-rays to rule out other lung diseases. Advanced emphysema slides show flattened diaphragm and hyperinflation. HEART: Hypertension Hypochromia and a dereased MCV indicates? Iron defieciency. Risks for comorbidities double with patients with hypertension. Patient comes in at least 2x, seated for 5 min, arm hanging. High risk population that should be targeted for risk of hypertension in primary prevention? Smokers. Think whats modifiable and whats not. C-Reactive protein indicates CVD as it shows inflammation of the vasculature tissue. Know LDL HDL Cholesterol Interaction Goals for treatment Dietary changes? Drug therapy: Statins: Libitor works in the liver, inhibits enzyme to produce cholesterol, decrease risk of mi and stroke. SE, muscle weakness, notify doc, lots of gas with it. Bile acids sequestreants.: binds to bile acids in the intestines, to ebe excreted . SE: abdominal discomfort, constipation, n/v. Take vitamins!! Because a lot of fat soluble vitamins will be secreted too! Fibric Acids fenofibrate: inhibit triglyceride synthesis and raise the HDLs.

SE: Rhabdomyolysis: break down of muscles. Then we are most concerned about the kidneys because they are filtering it out. Notify doc if you are having pain. Niacins: CO-enzyme for lipid metabolism. Decreased lipproteien and triglycerided synthesis. Side effect: Flushing of the face of the neck, (Vasodilation), orthostatic hypotension, gi upset that can be pretty severe. Give 300 mg aspirin for the flushing, 30 minutes before niacin dose. First line drug for hypertension: Thiazide type diuretics. Ace inhibitors: pril Beta blockers: olol Calcium antagonists. Know moa, side effects, patient teaching. Aldosterone blocking: Spironolactone Furosemide, Lasix, very high ceiling so you can give high doses. Rapid onset and potency. Within 2 hours you should see effects in there output. Thiazide diuretics can raise blood sugar levels in diabetics and need to be given carefully with the eldery. ADH: retain water Prostiglandins: pain and vasodilators, used to tx bronchoconstriction. For hypertension, we are trying to block the renin-angiotensin system Silent Killer: Complications: Left venticricular hypertrophy as blood is pushing harder against the constricted vessels. Primary hypertension: cant be linked to a deficit in another organ. Secondary hypertension: caused by another defective organ. Vascular system gets harder as you age: atherosclerosis. Coronary Artery Disease: Narrowing of the arteries in the heart, (coronary arteries). Starved myocardiu. Heart is not getting enough oxygen, and the heart cells die Angina: Tissue is starved

Know where the coronary arteries go Circumflex Left anterior descending: blood supply to left ventrical, widowmaker, clot left anteria descending, death Right main coronary artery: Know tests that can be done to determine if there are clots here. All coronary arteries are filled by r and le coronary arteries. Dont worry about dysrhythmias. When the aortic valve is open, the coronary arteries close and vice versa. When the heart is pumping more, the coronary arteries have less flow as they are being blocked by the aortic valve. Chest pain: heavy, crushing, Ischemia lack of o2 to the heart. Presenst differently in women. Is someone presents with chest painischemia Nitroglycerine: dilates the coronaries specifically, but will also have systemic and cerebral effects, thus give meds with gloves. Longterm Goal: Reduce o2 demand Increase supply Prevent mi Reduce symptoms which should improve quality of life. **Exercise, strengthen the heart. Acute Chest Pain. CABs Circulation airway, breathing. Emergent treatment: NOMA Nitro, Oxygen, Morphine, Aspirin. Put O2 on no matter what stats are, 2lpm nasal cannula. Jaw and neck pain is more indicative of chest pain. Vitals: increase in hr, and increase bp as a result. Stable vs unstable angina

Chest pain: 1. Assess what the chest pain is like, how long have you had it, any other symptoms, history? 2. MONA 3. Contact doctor. 4. Also get a stat EKG, as that has to be determined at time of chest pain Unstable angina, New onset, Changes in intensity, duration, or pattern of angina. Hypertension: Know different levels, different meds. Angina: Thorough assessment. Nitro: Every 5 min, 3x. After 5 min, headache, drop in bp. EKG tracing. Morphine to decrease anxiety, pain, and decrease work on the heart. Ischemia- blockage of blood flow and oxygen. Angina- pain from ischemia Infarction- tissue death Enzyme tests-CPK, Troponin

The PUMP
To meet the o2 needs of the body the heart has to work harder. CHF: Types: left sided, right sided, high output failure Blockages, valvular disfunction, atherosclerosis Best way to test: echocardiogram, soundwaves B-naturietic peptide C-reactie protein E-electrocardiogram Cardiac Catheterization C-reactive protein measurement of inflammation

BNP- B-type natuiuetic peptids any time atria is stretched, you secrete more of this hormone. Promotes urinary excretion of Na and water. (opposite of aldosterone). Helps rule out pulmonary embolism. People with BNP will have congestive heart failure. As tx starts, bnp will lessen Cardiac catheterization: risks: Right ventrical is a low pressure system. 15-25/0-8 Left ventrical is high pressure as it moves blood to aorta. Cardiac output=stroke volume x stroke rate. Ejection fraction- 55-60% Normal. Below is abnormal. Afterload: what the ventrical is pushing against. Pulmonary resistance right sided Vascular resistance left sided Preload: Volume left in ventricles, esp left ventricles. Measurement called LVEDP. Meds that reduce preload also reduce afterload. Higher heart rate decreased amount in ventricles. Blockage of the aorta increased preload. Pulmonary stenosis decreased preload. NYHA symptomatic classification 1- No symptoms 2- Minimal exertion 3- Moderate exertion 4- At rest Left Sided Heart Failure: Fluid backup in the lungs, pink frothy sputum. PND paroxysmal Nocturnal Edema.

Orthopnea Dyspnea on exhertion Decreased exercise tolerance Fatigue Dry hacking cough Unexplained confusion Abdominal discomfort. Ascites,heatic engorgement Third heart sound: too much volume due to turbulence (Kentucky Kentucky, Kentucky). Weak peripheral pulses, Angina due to decreased flow to the coronary arteries Right sided failure: JVD, jugular venous distension Enlarged liver and spleen Therapeutic Strategies: Neurohormonal blockade angiotensin blockers, ace inhihibitors Adequate hemodynamic management Maintenance of elelctrical stability Lifestyle mods and rehab Blunt neurohormonal response Beta blockers lols Synthetic BNP, natrecor drip Know about diuresis and titration levels Always think of potassium, because of diuretics Avoid: antiarhythmics Calcium channel blockers NSAIDS COPD right sided heart failure, eventually leading to left sided heart failure. Cor pulmonale BNP CRP Echo. Echo enlarged heart, decreased volume, high end diastolic, cardiac output will be low.

Peripheral Vascular disease Arterial: Dont do anything that is going to decrease blood flow. Venous: Clots. Intermittent claudication: aterial disease: pain on exheriton. Most common in lower extremities. Acute: clot Chronic: atherosclerosis Risk factors for Peripheral Arterial Disease: Legs: necrosis, pale, cold, hairless. Poikilothermy body temp that changes with environment. Chronic pain in lower back, buttocks. Can lead to arterial necrosis. Dx: arteriogram Rx: bypass surgery Chronic: patient teaching, reversible risks, exercise, antiplatelet meds, elective bypass. Bypass graft, taking a vein and attaching it to an artery so it can flow correctly. PTNT TEACHING; avoid standing/sitting too long. Inspect feet every morning because of paresthesia. DVT/VTE Virchows triad: stasis, vascular injury, hypercoagulability. Ankle discoloration and edema, brown pigmentation of the skin, prone to venous stasis ulcers. Capillaries get distended and break, red blood cells leak and break, and iron leaks there. Symptoms: dull ache, tightness or pain in calf. Physical assessment: edema, palpable cord Send for ultrasound to find out. Heparin: anti-Xa(10a). INR international normalized ratio of ptt. Or

INR of Pt. Goal 1.5-2x normal. Anti Xa 0.2-0.3 per protocol. (two to three times higher). Only normal for people on anticoagulants. Coumadin: look at PT, 1.5-2x higher. If person is normal, ratio should be 1. On anticoagulants, 2-3x higher. Heparin induced thrombocytopenia- 20% lower than normal For Heparin know How many units per hour is the ptnt getting? Labs every 6 hours. We take them off heparin drip and then switch them to Coumadin when they reach their 2-3x mark. Tx first episode 3-6months Second indefinitely. Stents, valve replacement, hx of clots, peripheral arterial disease, and a fib, (a fib can cause clots within the heart. Teaching therapeutic effects, injection procedures, avoid IM, pressure for 5 min.