Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Age Newborn 6-8 yrs Temp 36.8 axilary 37.7 rectal 37 oral 10 yrs 37 Teens 37 adults 37 Older adults (>70) 36 1-3 yrs Pulse 130 (80-180) 120 (80-140) 100 (75-120) 70 (50-90) 70 (50-90) 80 (60-100) 80 (60-100) Resp 35 (30-80) 30 (20-40) 20 (15-25) 19 (15-25) 18 (15-20) 16 (12-20) 16 (15-20) BP 73/55 90/55 95/57 102/62 120/80 120/80 Possible incr. diastolic Respiratory -Dry, irratative couch is characteristic of an upper resp tract infection of viral origin or may be a side effect of ACE inhibitors -Laryngotracheitis causes an irratative, high pitched couch -Trachial lesions produce a brassy cough -Severe or changing cough may indicate bronchosgenic carcinoma -Pleuritic chest pain accompanying coughing may indicate pleural or chest wall involvement Coughing at night possible on set of left-sided HF or bronchial asthma Cough in morning with sputum may indicate bronchitis Cough worsening when in supine may ne postnasal drip (sinusitis) Calcium Channel blockers -used to manage angina pectoris, dysrythmias, and hypertension Mechanism of Action -contraction of muscle is regulated by the amount of calcium ion inside of the cell, and when calcium enters the cell through channels in the plasma membrane, muscular contraction is initiated. -relax arterioles and reduce peripheral resistance to decrease BP -acts large and fast. (decreases BP fast). Good in crisis! -not for stable theory -Amiodipine (norvasc), Diltiazem (Cardizem, Dilecor XR), Nifedipine (Adalat, Procardia), Verapamil (Calan, Isoptin, Verelan, Covera) Angiotension Converting Enzyme Inhibitor (ACE Inhibitors) PRIL -ACE Inhibitors are used to manage hypertension, heart failure, and myocardial infarctions Mechanism of Action -Block the conversion of angiotension I and angiotension II, which decreases BP by lowering resistance (through vasodilatation) and decreases blood volume (by preventing the secretion on aldosterone by the adrenal cortex). * (Helps with fluid). -Enalapril (Vasotec), Lisinopril -after load reduction -reduces sodium and water retention (causes diuretic effect) -does not have effect of rate Beta Blockers OLOL -used to manage hypertension and myocardial ischemia (angina). There is a cardioprotective effect to prevent MI Mechanism of Action -action is the decrease of HR, and through reduction of myocardial conduction rate and contractility. Shrinks cardiac hypertrophy. Drops cardiac workload. -Can cause fluid retention. Can cause fatigue -Atenolol(tenormin), bisoprolol(zebeta), metoprolol(toprol, lopressor), Propanolo(Inderal), timolol(Betimol) -Decrease preload (cardiac), decrease after load (peripheral), decrease HR and cardiac workload, decrease BP, shrinks large hearts. Causes fluid retention Digoxin (Cardiac Glycosides) -Used in management of CHF, tachyarrythmias: atrial fibrillation and atrial flutter (slows ventricular rate) Mechanism of Action -Increases cardiac output (positive inotropic effect), and slowing of the HR (negative chronotropic effect) -increases the force of myocardial contraction -Digoxin, Digitoxin (more prolonged half-life) -PO- onset 30-120 min, peak 2-8 hr, duration 2-4 days -IM- onset 30 min, peak 4-6 hr, duration 2-4 days -IV- onset 5-30 min, 1-4 he, 2-4 days -SE: fatique, bradycardia, anorexia, nausea, vomiting Nitroglycerine (antianginals) -used in the management of angina, and useful in the management of HF -Relax both arterial and venous smooth muscle. - Increases cardiac output. Reduction of BP -dilation of the coronary arteries to improve perfusion of myocardial tissue (particularly helpful when angina is due to coronary artery spasm). -Produces vasodilatation. Helpful with angina - SL- onset 1-3 min, peak unknown, duration 30-60 min -PO-ER- onset 40-60 min, unknown, duration 8-12hr -TD-onset Patch 40-60 min, peak unknown, duration 8-24hr -SE: dizziness, headache, hypotension, tachycardia P = Provokes What causes pain? What makes it better? Worse? Q = Quality What does it feel like? Is it sharp? Dull? Stabbing? Burning? Crushing? R = Radiates Where does the pain radiate? Is it in one place? Does it go anywhere else? Did it start elsewhere and now localised to one spot? S = Severity How severe is the pain on a scale of 1 - 10? T = Time Time pain started? How long did it last? Other questions to ask and look for.... Does it hurt on deep inspiration? Activity @ onset? Any history of pain? Is it the same? Different? Any family history of heart disease lung problems, stroke or hypertension? Check LOC. Pupils? JVD? Midline trachea? Any recent trauma? Post Anesthetic Activity – able to move four extremities voluntarily or on command - Able to move two extremities voluntarily or on command Unable to move extremities voluntarily or on command Respiratory- able to deep breath and cough Dyspnea or limited breathing Apneic BP Consciousness- fully awake Arousal on calling Not responding O2 sats- >90% on room air Needs 02 for > 90% <90% even with o2 Wound Exudate Serous- clear, watery plasma. Serum does not contain blood cells or platelets. Ex. Fluid from a blister Serosanguineous- Thin, water drainage that is blood-tinged. Commonly seen in surgical incisions Sanguineous- blood drainage. Larger amounts may indicate hemorrhage; this type frequently seen in open wounds. Purulent- Thick drainage that contains pus. Purulent drainage caries in color depending partly on the organism in the pus and may be green, yellow or brown. Dressing – dry and clean Wet but marked and not increasing Growing area of wetness Pain- pain free Mild pain handled by oral meds Severe pain requiring parenteral meds Ambulation – able to stand up and walk *straight Vertigo when erect Dizziness when supine Pasting-feeding- able to drink fluids Nauseated Nausea and vomiting Urine output- has voided Unable to void but comfortable Unable to void and uncomfortable