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141 Cards in this Set
- Front
- Back
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Sympathetic Nervous System
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- alpha and beta stimulated by norepi and epi (in response to ANY stress)
- results in: -- increased HR -- increased vasoconstriction - responsiveness decreases with aging |
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DO NOT given non-cardioselective betal blockers to?
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people with lung disease/asthma
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Medication management goals for HTN
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BP 140/90
BP 130/8- if renal disease or diabetes |
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Isolated Systolic HTN
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SBP >140 (usually greater than 160) and DBP < 90
- more common in elderly due to decreased elasticity of vessels |
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Pseudohypertension
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- caused by athersclerosis of the larger arteries
- Higher cuff pressures than in vessels - Need arterial line to get accurate BP |
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Causes of HTN crisi
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- exacerbation of uncontrolled HTN
- renvascular HTN (overproducing renin --> RAA) - Preclampsia, eclampsia - Phechromocytoma (medullca timor overproducing epi) - Cocaine, amphetamines - Rebound HTN from abruptly stopping Catapress or beta blockers - Necrotizing vasculitis Head injury (pressure on brain stem) Acute aortic dissection |
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Hypertensive Emergency
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- sudden and abrupt elevation pof BP (especially DBP >120, my be >220/40)
- Develops over hours or days - rise more significant than value - life threatening/end organ damage (especially to CNS--if kidneys aren't the cause than it can cause kidney damage also) |
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Hypertensive urgency
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bp values equal to HTN emergency
- no clinical evidence of end organ damage (no HA, no signs of stroke, no cardiac pain, normal creatinine) - rate of rise important Chronic hypertensive pts may tolerate this better |
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Hypertensive encephalopathy
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Complication of HTN emergency
- rise in BP - HA (poor brain perfussion) - Nausea (increased ICP) - vomiting (increased ICP) - vision changes/transient blindness - seizures - confusion/stupor - coma The encepahalopathy increases cerebral permeability leading to cerebral edema and retinal papilledema also |
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Other HTN emergency complications besides encephalopathy
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- Intracranial hemorrhade
- subarachnoid hemorrhage - Left ventricular failure (pulmonary edema, cardiogenic shock) - MI - Renal failure - Aortic dissection - Retinopathy--> blindness |
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MAP=
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DBP + 1/3 Pulse pressure
Pulse pressure is S-D |
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Treatment of HTN emergency
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- Lower MAP 25% in first hour
- when stable, less than 160/100-110 over next 2-6hrs - additional gradual decrease over 24-48 hours ** Ask Dr what are BO he/she would like * MUST LOWER SLOWLY or perrfusion to vital organs can be deminished will cause stroke, MI, and decreased renal perfussion (which will cause a BP increase with renin release) - bedrest - monitor BP q 2-3 min- makes ure they are recorded, with timer and alarm - arterial line or NIBP monitor preferred - prevent hypotension - monitor renal lab paramenters (creatinine, BUN) - Monitor urinary output - ECG monitoring for ischemic changes (ST and T) and dysrhythmias - Neurologic assessment (FULL neuro checks q1h) - Cardiopulmonary assessment q1h (signs of CHF, pulmonary edema, breath sounds) |
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IV vasodilators for HTN emergency
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- Nitroprusside (wrapped in foil, cyanide)
- Nitrglycerine (vented tubing, glass) Hydralazine (common in pregnancy, OB) Nicardipine (CCB) Labetolol (BB) Enalapril (ACE) |
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HTN Urgency treatment
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- often managed with oral meds
- requires frequent follow-up if not hospitalized - common meds (Catapress, Captopril, Labetolol) - education on BP home monitoring and what parameters to call MD or 911 |
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Causes of endothelial damage
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- smoking
- HTN - DM - Infection (Chlamydia, herpes systemic infection) - Elevated homocystein levels - Local inflammation (c-reactive protein is marker) |
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Right coronary artery (RCA)
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Right lateral wall
Right ventricle Right atrium Inferior part of LV SA node AV node * conduction changes are in the form of heart blocks |
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Left main artery breaks into-->
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Left anterior desceding (LAD) and Left Circumflex artery
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Left Anterior descending artery -->
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Front anterior wall of heart to the apex, includes left ventricle, septum, chorday tendinae, papillary muscles (shuts valve) and right ventricle
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Left circumflex -->
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Lateral wall and posterior wall of LV
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Devlopmental stages of CAD
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Fatty streak --> Fibrous plaque --> Complicated lesion (gets bigger and ruptures)--> platelet aggregation
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Fatyy streaks
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- lipoproteins enter intima
- yellowish, flat, lipid rich - Monocytes develop into macrophages - Lipid rish cells are called "foam cells" ** First sign of atherosclerosis |
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Fibrous plaque (Atheroma)
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- white, pearly elevations of intima lining
- Damage to intima liberates platelet derived growth factor - Proliferation of smooth muscles cells - Stimulates movement of smooth muscle cells from media to intima layer - Fibrous cap forms from connective tissue and low-density lipoprotein (LDL) - necrotic core forms from inadequate blood flow |
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Advanced/Complicated lesion
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- Rupture of the fibrous cap
- Thrombus formation with gradual increase in size - Rupture of plaque starts clotting cascade |
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Vitamin B12, B Complex, folic acid
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Homocysteine levels can be reduced with this, cardiac pts should be on it
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DASH diet
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low sodium
monounsaturated fat dominant diet (nuts, olive oil, canola oil, limit polyunsaturated fats, eliminate saturated fats) - Increase complex carbs (fruits, high fiber foods) - Omega 3 Fatty acids --> inhibit platelets (important to know if pt going to surgery) and drop triglycerides ---fatty fish (tuna, salmon) ---Linoleic acid (soybean, walnut, flaxseed, tofu) |
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LDL levels
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<100 optimal
160-189 High >/ Very high |
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Total Cholesterol levels
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<200 Desirable
>/ 240 High |
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HDL Cholesterol levels
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<40 Low
>/ 60 High |
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High risk
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10 yr risk >20%
HAS cad OR RISK EQUIVALENT - goal- <100 (<70 optimal) |
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Moderately High risk
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10-20% 10 yr risk
2 or more risk factors but NO CAD -goal- LDL <130 mg/dL with optimal <100 mg/dL |
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Moderte risk
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<10% 10 yr risk
2 or more risk factor but no CHD goal- LDL <130 mg/dL |
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Low to moderate risk
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0-1 risk factor
<10% 10 yr risk goal- <160 mg/dlL |
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Statins
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- lower LDL
- S/E- rhabdomyopathy and liver |
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Fibrates
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----fibra
- lower triglycerides |
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Niacin
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Increase HDL
- S/E- flushing and increase in blood sugar |
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Bile acid sequestrants and Zetia
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absorb cholesterol from gut
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Fish oil
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Decreases triglycerides
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Aspirin
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pts with high risk conditions (like diabetes), use framingham shoul dbe on aspirin therapy
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Plavix
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Common after cardiac procedures
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Symptoms of blockage occurs when?
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when 70-75% blocked and usually lasts 3-5 min (myocardial damage occurs by 20 min)
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Chronic Stable Angina
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predictable
- anticipated and pre-treated - relieved by rest and nitroglycerine |
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Unstable Angina
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- not predictable
- not related to activity, occurs at night - requires more tx to make it go away |
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Prinzmetal (Variant) angina
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spasm of coronary artery
- rare- people with migraines or Raynaud's more prone to it -cocaine and meth do this too but not called Prinzmetal -Calcium Channel blockers can help with this |
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Nocturnal Angina
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occurs at night (not necessarily while sleeping or lying down)
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Angina decubitus
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only when person is lying down
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Clinical manifestations of Chronic Stable Angina
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- pain lasts 3-5 min
- subsides when precipitating factors relieved - pain at rest in unusual ** ECG reveals ST segment depression - some may have ST elevation * ST elevation AND depression are both a worry |
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PQRST assessment of angina
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P- precipitating events (rest v activity)
Q- Quality of pain (crushing, ache, indigestion, etc.) R- Radiation of pain (cardiac often down L arm or back, abdomen, scrotum even, anywhere) S- severity of pain (pain scale rating) T- timing (what doing and how long did it last) |
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Silent Ischemia
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No symptoms
More common with DM (secondary to autonomic diabetic neuropathy) - High risk for sudden cardiac death (if u don't feel it u don't treat it) |
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Q wave
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Always abnormal but may indicate OLD myocardial damage
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ST segment
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- should be isoelectric
Elevation = myocardial injury Depression = Myocardial ischemia Both = RISK FOR SUDDEN DEATH! |
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Inverted T wave
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My indicate MI or ischemia, but other things can cause this as well
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3 goals of managing chronic stable angina
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- treat atherosclerosis
- improve oxygen supply - reduce oxygen demand |
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Nitrates for Angina
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- enhance blood flow (dilate coronary arteries)
-- decrease work load of heart (Dilate peripheral blood vessels --> venous dilation, shunts blood to extremeties (helps preload and afterload) short acting- sublingual - nitroglycerine spray or tab Long acting - Imdur - NTG patch |
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S/E of nitrates
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- HA, hypotension (ED drugs will be severe!! and alpha blockers for prostate)
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Beta blockers for Angina
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- preferably cardioselective (atenolol, labadelol)
- decrease contractility, rate, SVR, BP --> give heart and arteries time to fill - decrease morbidity and mortality |
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S/E of beta blockers
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- bradycardia
- HypoTN - Bronchiole constriction (wheezing in non cardioselective) - May reduce awareness of hypoglycemia in non-cardioselective ** must be tapered off- or will have rebound HTN leading to crisis |
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Calcium Channel Blockers for angina
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- cause systemic and coronary vasodilation
- decrease contractility --> could precipitate HF - nefedipine (procardia) - Verapamil (Calan) - Diltiazem (Cardizem) - Nicardipine (Cardene) |
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S/E of calcium channel blockers
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- could precipitate HF
- Potentialtes Digoxin |
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Ace inhibitors for angina
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- reduce vasoconstriction and aldosterone release
- Captopril - Enalapril - Lisinopril - Accupril |
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S/E of ACE inhibitors
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may produce cough, first dose hypotension, hyperkalemia, angioedema
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Ranolazine (Ranexa) for Angina
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- Sodium current inhibitor
- Should be used in combination with amlodipine (Norvasc), Beta blockers, nitrates - affects cytochrome system **Avoid with significant liver impairment |
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Reversible defect on dx
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needs a cath
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Nonreversible defect on dx
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dead tissue
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Thallium stress testing
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when symptoms occur, injected with radioactive dye and multiple imaging (24h later), nucleotide collects in healthy tissue
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Persantine Thallium
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for pts that can't tolerate exercising
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Percutaneous Coronary Interventions (PCI)
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-angioplasty (PCA)--> balloon (reocclusion risk is VERY high, especially if smoke 100%)
- stent (helps to prevent reocclusion) - atherectomy --> roto rooter, shaves plaque off * recommended for UNstable angina before pt infarcts - pt must be candidate for surgery |
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Nursing care for PCI (Percutaneous Coronary Interventions)
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- monitor for restenosis/ischemia
- Bedrest--> prevents arterial bleeding (duration depends on site) - Compression of entry site - Immobilization of affected limb Site assessment- bleeding, hematoma, monitor pulses distal to site of insertion - antiplatelet therapy - HOB </ 30 degrees if femoral access - bed rest if had femoral Monitor: bilateral peripheral pulses, color, sensation distal to insertion site Monitor: cardiac rhythm I&O (encourage fluids and IV) Observe for adverse reaction to contrast media *Monitor creatinine, especially in pts with renal insufficiency or metformin (metform day of anf 48h after) * mucomyst helps defuse dye |
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Most serious complication of Percutansous coronary interventions
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vessel dissection and coronary artery rupture
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Vessels for CABG
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Saphenous vein
Internal mammary artery (LIMA, RIMA) Radial artery Arteries are better cause they are stretchy and can tolerate higher pressures of blood flow |
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CABG indications
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- Unstable angina with no success with other tx
- Acute MI (best if can recover from MI a little first) - Failure or PCI - Left main disease (can't put stents in left main) |
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Complications of CABG
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- bleeding related to platelet damage
- Anemia related to RBC damage - F/E imbalances - Hypothermia - Cognitive dysfunction - Post pumps syndrome- depression or cognitive changes - Dysrhythmias (atrial are most common per book) - Impaired contractility, low CO - Intraoperative MI - Pericardial tomponade (sac of heart fill with blood and can't contract) - Respiratory failure and insufficiency - Pain - Emboli, stroke - Sternal wound infection - Harvest vessel site infection - renal impairment (from drop in renal perfusion) - GI dysfunction (drop in perfusion) - Impaired peripheral circulation - Infection (can get osteomyolitis of sternum) - Post-cardiotomy delirium - poor nutrition status |
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Nursing Interventions post CABG
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- Assess for hypovolemia (chest tube and urine drainage)
- Monitor for hypotension (fluids and vasopressors as ordered) - Monitor hemodynamics (CO, CI, treat per protocols) - Rewarm gradually- (prevent hypothermia which increases O2 demands) - Lab monitoring (F/E, H/H, Creatinine/BUN, Coagulation studies (bypass causes coagulation) - Pain management (Cough and deep breath, turning, increases BP and HR) - Monitor for complications - wean from mechanical ventilation and extubate - C&DB q2h while awake (support sternal wound) - Assess wounds - Incisional care as per protocol - glucose control in DM - gradually increase activity - DVT prophylaxis - Emotional support (pt and family) - Cardiac rehab |
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Nurse must monitor for what CABG complications
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- Intraoperative acute MI
- Dysrhythmias - HF- breath sounds, edema, S3 - Cardiac tamponade - Thromboembolism, DVT - Impaired Renal Function - Pneumonia - Pneumothorax - Pleural Effusion - Cerebral Ischemia - Stroke |
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MIDCAB (Minimally invasive Direct CAB)
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- "Peripheral" bypass with balloon crossclamping aorta
- fewer complications and quicker recovery - 1 or 2 bypass on anterior |
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Transmyocardial Laser Revascularization
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- laser channels into ventricle
- Goal is to increase perfusion of heart muscle from inside out - nonsurgical, non PCI candidate with persistent pain - may take 6 months for relief of symptoms - mixed results from clinical trials |
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Acute Coronary Syndrome includes:
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- Unstable Angina- partial occlusion
- Non ST segment elevation MI (troponins go up but don't see ST elevation, warning for a BIG MI)- partial occlusion - ST segment elevation MI (STEMI) (extensive muscle damage leading to the ST elevation on ECG- full occlusion |
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Unstable angina
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New onset
Occurs at rest Has a worsening pattern **Unpredictable and represents a medical emergency |
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Q wave m non Q wave MI
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Q wave- more serious and shows more damage, total occlusion of coronary artery with thrombus
non Q wave- pt may have a normal ECG and have elevation of cardiac enzymes. Partial occlusion of coronary artery |
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MI causes
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platelet aggregation/thrombus
Spasm |
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time of MI
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>20 min of sustained ischemia causes irreversible myocardial cell death (necrosis)
Necrosis of entire thickness of myocardium taken 4-6 hrs |
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Acute MI clinical manifestations
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Change in anginal pain
-severe, crushing, squeezing, pressure - may radiate - unrelieved with rest or nitrates - may be atypical, especially in women Pale and diaphoretic (sympathetic stimulation, hypotension) Dyspnea Syncope N/V (vagal stimulation, sympathetic) *Dysrhythmias -- Bradycardia in Inferior (right) MI -- ventricular dysrhythmias in Anterior MI and Lateral MI New S3 (may indicate HF) or S4 New murmur (may indicate papillary muscle damage) Pulmonary congestion Fever (activation of inflammatory response) |
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S/S of Acute MI
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- be alert for atypical
- 12 lead ECG: ST ELEVATION followed by a Q wave or - ST depression (non q wave MI) - compare with prior ECGs (Q waves may indicate old damge) - Elevated cardiac enzymes (CPK-MB) - Elevated serum troponin I/T, myoglobulin - Enzymes need to be assessed serially (q8h x3) - early cardiac cath and intervention **most significant is ST elevation **Secondary is the Q wave (may or may not be acute) |
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Nursing goals in acute MI
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- maintain CO
- treat pain--> morphine helps in pain, anxiety, and vascular pooling - Assess for complications - Increase activity tolerance - Relieve anxiety - Ongoing and discharge teaching |
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Complications of acute MI
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- Dysrhythmias
- SUDDEN CARDIAC DEATH - Congestive heart failure, cardiogenic shock - Ventricular aneurysm (weakness in wall, rupture) - Papillary muscle dysfunction (Mitral valve incompetency) - Dressler's syndrome - Pericarditis - Extension MI ** Must be monitored for 6 weeks after MI (rupture especially) |
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Dressler's syndrome
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Pericarditis symptoms 4-6 weeks post MI
- chest pain is differnt - hurts worse with a breath and positional - can point to a specific spot where it hurts - possible increased SED rate |
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Emergency management of Acute MI
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- pain relief (morphine, nitroglycerine)
- OXYGEN- #1 - Emergency PCI procedures of cath (PCA is preferred to PCI or TPA/thromblytics) - Drugs affecting platelets (ASA< glycoprotein, IIb/IIIa inhibitors) - BEta blockers (not immediately because it decreases contractility, etc by inhibiting sympathetic NS but should discharge on them - Nitrates - ACE inhibitors |
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Inferior wall changes (RCA ischemia) on ECG
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Lead II, III, AVF
- ST elevation or depression - bradycardia and SS3 Right sided HF |
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Anterior Wall MI changes (LCA ischemia) changes in ECG
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V 1-3 leads
Monitor for ventricular rhythms and Left sided HF |
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S/S/ of pericarditis
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- common after MI 2-3 days after
- aggravated chest pain with coughing, inspiration, and movement of upper body - different type of pain then MI - friction rub (diaphragm of steth at mid to lower sternal border) - Fever may be present |
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CK levels/ CK-MB
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- rise at 6h after MI
- peak at 18h - return to normal 24-36 h |
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Troponin levels
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- CTnT and CTnI
- 4-6h after IM onset - peak at 10-24h - return to baseline over 10-14 days |
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Myoglobulin
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- 2 h after MI onset
- peaks in 3-15h - lacks cardiac spcificity - return to normal in 24 h (excreted rapidly by kidneys) |
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Thrombolytic Therapy
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*Time is muscle--> 6 HOUR WINDOW
Meds: - tissue plasminogen activator (t-PA) - streptokinase Heparin and glycoprotein IIB/IIa inhibitors used in conjunction (ie: Integrilin) |
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Absolute Contraindications for Fibrinolytic therapy
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- Active internal bleeding or bleeding diatheses (excluding menstruation)
- Known hx of cerebral aneurysm or arteriovenous malformation - Known intracranial neoplasm (primary or metastatic) - Previous cerebral hemorrhage - Recent (with in past 3 mo) ischemic stroke - Significant closed head or facial trauma within 3 mo - Suspected aortic dissection |
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Relative contrainidcations of fibrinolytic therapy
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- Active peptic ulcer disease
- Current use of anticoagulants - Pregnancy - Prior ischemic stroke > 3mo, dementia, or known intracranialpathology not covered in absolute contraindications - Recent (within 3 weeks) surgery (including laser eye) or puncture of noncompressible vessel - Recent internal bleeding (2-4wks) - Serious systemic disease (advanced/terminal cx, severe liver/kidney disease) - Severe uncontrolled HTN (BP > 180/110) on presentation or chronic severe poorly controlled HTN - Traumatic or prolonged (>10min) CPR |
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Bedside Tx of MI
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- monitor for recurrent chest pain--> could indicate extension of MI
- stop activity - Oxygen - STAT ECG (pre and post ntg) - Nitroglycerine (sublingual after ECG) - Morphine - Nitroglycerine IV - Intra-aortic balloon pump (critical care) |
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Heparin lab
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PTT (1.5-2 x normal= about 60-80)
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Coumadin lab
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INR 2-3
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Thrombolytic meds
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Streptokinase
tPA Retavase |
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Assessment of MI pt
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chest pain, cardiac monitoring
Apical pulses - Gallops (s3)- CHF - Rubs- pericarditis - Murmurs- valvular diseases/papillary muscle damage Lungs- crackles, wheezes, rhonchi (make sure not in acute HF especially if have Left V damage) Feet-edema |
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MI's don't kill patients but_____ does
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dysrhythmias
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Sudden Cardiac death (SCD)
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Unexpected death from cardiac issues, abrupt disruption in cardiac function, resulting in loss of CO and cerebral blood flow
- death usually within an hr of onset of acute symptoms (angina, palpitations) ***DON'T DRIVE SELF TO ER IF HAVING CHEST PAIN*** - usually outside of hospital deaths - CAD accounts for about 80% of all SCDs |
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most common cause of sudden cardiac death
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- ventricular dysrhythmias (ie: v- tach)
--less commonly caused by left ventricular outflow obstruction (aortic stenosis) |
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Primary and other risk factors for Sudden cardiac death
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Primary
- Left ventricular dysfunction (EF 30%, cardiomyopathy) - Ventricular dysrhythmias after MI Other - male (Especially AA) - family hx of premature atherosclerosis - tobacco use - DM - Hypercholesterolemia - HTN - Cardiomyopathy (muscle alrge and alters electrical system of heart) |
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Cardiac rehab phases
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Phase I -hospital
Phase II- Early Recovery (2-12 weeks following discharge) Phase III- Late recovery (maintenance) |
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Post MI education
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- S/S angina/MI and emergency management
- Risk factor reduction -Therapeutic diet - Pulse monitoring - Medications - Activities (HR 60% of age predicted max) - post op care - s/s of depression and adjustments |
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Chronic Compensation in Chronic HF
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- dilation
- Hypertrophy - SNS stimulation - Hormonal response (RAA) HF is a neuroendocrine disorder |
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#1 reason peopls admitted and readmitted to hospital
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Acute Decompensated Heart Failure
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Manifestations of Acute Decompensated HF
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- Fatigue
- Dyspnea - Tachycardia (from hypoxia) - Edema - Nocturia - Dusky colo of skin - behavior changes (cerebral anoxia) - Chest pain - Weight gain (****VERY Important to monitor) |
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Complications of Acute Decompensated Heart Failure
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- PLeural effusion
- Dysrhythmias (irritable V cells from hypoxia or from being stretched out) - Left ventricular thrombus - Hepatomegaly - Renal failure |
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Most useful diagnostis for Acute decompensated HF
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X-Ray- can see fluid in lungs
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Other dx for Acute HF
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ECG
Echo Cardiac cath (Swann Gans catheter)- to measure pressures in heart BNP level |
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Treatment for Acute Decompensated HEart Failure
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Increasing inotropic Activity of Heart (pump)
-digitalis and other meds Decreasing preload (fluid) - morphine - diuretics - vasodilators - diet (low salt, fluid restriction) Decreasing afterload (pressure/resistance) - BP reduction - Tx of aortic or pulmonic stenosis |
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Cardiogenic shock
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pump failure, usually due to 40% loss of ventricle
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Signs of cardiogenic shock
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Hypotension
Tachycardia low Urine output (<30ml/h) Cold clammy skin Agitation Tachypnea Thirst |
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Treatment for Cardiogenic shock
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- Decrease heart O2 demand (decrease preload and afterload)
- Supply O2 - Monitor BP - Intraortic balloon pump - ICU |
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Cardiomyopathy categories
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Dilated
Hypertrophic Restrictive |
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Dilated cardiomyopathy
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- Normal wall thickness (does not thicken like HF)
- Poor contractility - Pump Failure - More Common in men Cause is unknown, alcohol, or chemo |
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Hypertrophic Cardiomyopathy
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- small chambers --> poor filling --> heart failure
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Restrictive cardiomyopathy
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- rare
- fibrotic walls --> decreased contractility --> HF |
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Treatment of choice for refractory end stage HF, inoperable CAD, and cardiomyopathy:
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Cardiac transplantation
- goal is to identify pts that would most benefit from a new heart |
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Primary complications of cardiac transplant
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The first year:
#1- Infection #2- Rejection #3- renal (immunosuppressants for nephrotoxic) Beyond the first year: malignancy (especially lymphoma) and coronary artery vasculopathy are major causes of death from immunosuppression |
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Rejection monitoring
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Endomyocardial biopsies:
- weekly for the first month - monthly for the following 6 mo - yearly therafter Heartsbreath test is used along side biopsies to assess for organ rejection |
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Infective Endocarditis
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- cardiac valves
- Treated with PCN - Vegetations consists of fibrin, leukocytes, platelets, and microbes - loss of elasticity --> breaking off and embolization **Infection--> sepsis (staph or strep usually) |
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Symptoms of endocarditis
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Low grade fever
chills weakness malaise fatigue anorexia arthralgias myalgias back pain weight loss HA Clubbing of fingers Splinter hemorrhages in nail beds Petechiae from microembolization in conjuncitvae, lips, buccal mucosa, ankles, feet, antecubital and popliteal areas -Osler's nodes (painful, tender, red or purple, peasize lesions) found on fingertips or toes - Janeway's lesions (flat, painless, small, red spots on palms and shoes) - Roth's spots (retinal hemorrhagic leasions) - murmurs |
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Pericarditis causes
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-idiopathic
- coxsakievirus B group is most common viral cause - Uremia - TB - Neoplasm - Trauma -MI - Resslers syndrome |
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Pericarditis
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Inflammation of pericardial sac
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S/S of pericarditis
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- pain on inspiration (chest pain mimicking angina)
* pericardial friction rub * Intensity caries with position (book states worse when lying down) |
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Pericarditis labs
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WBC, ESR, CRP (all indicators of inflammation)
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Treatment of pericarditis
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- Indentify underlying problem
- Antibiotics - Steroids (for special pt only, Lupus) - NSAIDS, Aspirin - Colchicine - Pericardiocentesis for tamponade - Surgery?? (Pericardial window) |
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Myocarditis
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Inflammation of the myocardium (may be assiciated with pericarditis)
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Causes of myocarditis
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- Viruses (coxsackie virus)
- Bacteria - Fungi - Raiation - Drugs/chmicals - Autoimmunity |
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Symptoms of myocarditis
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Early: General viral illness
Mid: pleural chest pain, pericardial friction rub Late: CHF, angina, edema, Sudden cardiac heatlh |
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Treatment for Myocarditis
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**No definitive tx
- digoxin diuretics - Diuretids - Decrease afteroad - Anticoagulationif EF is low Immunosuppression to decrease inflammation |
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Rheumatic Fever/Heart DIsease
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Rheumatic fever usually caused by group A strep->> Rheumatic heart disease -->>
pancarditis endocartitis pericarditis with adhesions can afffect other aparts of the body |
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Major criteria for Rheumatic Fever/Heart disease
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-Carditis (murmurs, cardiac enlargment, pericarditis)
- mono or polyarthritis* - Sydenham;s chorea (involuntary movements of face, limbs, muscle weakness, and disturbances of speech and gait) - Erythema marginatum (bright pink macular lesions on trunk and proximal extremities) |
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Minor criteria for Rheumatic Fever/Heart DIsease
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- fever, increased WBC, ESR, CRP
- evidence of recent prior infection |
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Treatment for Rheumatic Fever/Heart Disease
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no single test for dx
- bed rest - antibiotics - steroids - salicylates - NSAIDS |
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Manifestations of Peripheral Vascular Disease
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- Intermittent Claudication
- male sexual dysfunction - Parasthesia - Skin becomes thin, shiny, and taut - Loss of hair on lower legs - Diminished pulses - Elevation pallor/reactive hyperemia/dependant rubor - Rest pain |
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Dx for peripheral vascular disease
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- doppler
**Segmented BP (thigh, below knee, ankle)-- drop of 30mm Hg= PVD - Ankle-brachial index (ankle Systolic by brachial systolic) **Normal = 0.91-1.3 **Mild PAD = 0.71-0.90 **Moderate PAD= 0.41-0.70 ** Severe PAD = <0.40 |
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Priority nursing interventions for carotid endarterectomy
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- general surgical management
- cardiac monitoring ***MONITOR NEURO STATUS (stroke risk) - stroke education |
