Oxygen Transport
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| What are the clinical manifestations of hyperkalemia (>5.0)? | irritability, anxiety, abdominal cramping, diarrhea, weakness of lower extremities, paresthesia, irreg. pulse, cardiac arrest if sudden or severe
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| What would a patient with hyperkalemia (>5.0) look like on an ECG? | Tall, peaked T wave; prolonged PRI, ST segment depression; loss of P wave; widening QRS; Vfib, ventricular standstill
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| What are some causes of hyperkalemia (>5.0)? | Excess K intake (excess. rapid parenteral admin., K containing drugs & salt subs.; shift of K out of cell (acidosis, tissue cat.); fail to eliminate K (K sparing diuretics, renal disease, ACEI, NSAIDS, adrernal insuff.)
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| What are some causes of hypokalemia (<3.5)? | K loss (diarrhea, vomiting, NG suction, diuretics, Mg depletion, dialysis, diaphoresis); shift of K into cell (inc. insulin, alkalosis, tissue repair, inc. epi -stress); lack of K intake (starve, diet low in K, fail to include K in parenteral fluis if NPO
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| What are the clinical manifestations of hypokalemia (<3.5)? | fatigue, muscle weakness, leg cramps, N/V, paralytic ileus, soft, flabby muscles, paresthesias, dec. reflexes, weak, irreg. pulse, polyuria, hyperglycemia
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| What would a patient with hypokalemia (<3.5)look like on an ECG? | ST segment depression; flattened T wave, presence of U wave, prolonged QRS, ventricular dysrhythmias (PVCs); bradycardia
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| What are some causes of hypercalcemia (>10.2)? | Inc. total Ca (mult. myeloma, malignancies w/bone metastasis, prolonged immobile, hyperparathyroidism, Vit D overdose, thiazide diuretics; Inc. ionized Ca (acidosis)
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| What are the clinical manifestations of hypercalcemia (.10.2)? | lethargic, weakness, depressed reflexes, dec. memory, confusion, personality changes, psychosis, anorexia, N/V, bone pain, fractures, polyuria, dehydration, nephrolithiasis, stupor, coma
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| What would a patient with hypercalcemia (>10.2) look like on an ECG? | shortened ST segment; shortened QT interval; ventricular dysrhythmias; increased digitalis effect
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| What are some causes of hypocalcemia (<8.6)? | Dec. total Ca (CKD, elevated Phos, primary hypoparathyroidism, Vit D def, Mg def, acute pancreatitis, loop diuretics - furosemide, chronic alcoholism, diarrhea, dec. serum albumin; dec. ion. Ca (alkalosis, excess admin of citrated blood)
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| What are the clinical manifestations of hypocalcemia (<8.6)? | easy fatigability, depression, anxiety, confusion, numbness and tingling in extremities & around mouth, hyperreflexia, muscle cramps, Chvostek's & Trousseau, laryngeal spasm, tetany, seizures
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| What would a patient with hypocalcemia (<8.6) look like on an ECG? | elongation of ST segment; prolonged QT interval; ventricular tachycardia
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| How would you treat a patient with hyperkalemia (>5.0)? | stop oral & parenteral K, inc. elimination of K w/diuretics, dialysis, & kayexelate; force K from ECF to ICF w/IV of regular insulin along w/glucose, or IV bicarbto correct acidosis; IV calcium gluconate to protect heart from dysrhythmias
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| How would you treat a patient with hypokalemia (<3.5)? | Give oral or IV KCl supplements and increase intake of K
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| How would you treat a patient with hypercalcemia (>10.2)? | with Loop diuretics (furosemide-Lasix) and hydrating the pt with isotonic saline infusions
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| Air in the pleural space. | pneumothorax
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| What are the CM of pneumothorax? | dyspnea, dec. movement of involved chest wall, diminished or absent breath sounds on the affected side, hyperresonance to percussion
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| How do you treat a pneumothorax? | chest tube insertion w/flutter valve or chest drainage system
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| Blood in the pleural space, may or may not occur in conjunction w/pneumothorax. | hemothorax
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| What are the CM of hemothorax? | dyspnea, diminished or absent breath sounds, dullness to percussion, dec. Hgb, shock depending on blood volume lost
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| How do you treat a hemothorax? | Chest tube insertion w/chest drainage system. Autotransfusion of collected blood, treatment of hypovolemia as necessary.
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| Air in pleural space that doesn't escape. The increased air in the pleural space shifts organs and increases intrathoracic pressure. | tension pneumothorax
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| What are the CM of tension pneumothorax? | cyanosis, air hunger, violent agitation, tracheal deviation away from affected side, subcutaneious emphysema, neck vein distention, hyperresonance to percussion
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| How do you treat a tension pneumothorax? | Medical emergency; needle decompression followed by chest tube insertion w/chest drainage system.
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| Fracture of two or more adjacent ribs in two or more places w/loss of chest wall stability. | flail chest
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| What are the CM of flail chest? | Paradoxic movement of chest wall, respiratory distress. May be associated hemothorax, pneumothorax, pulmonary contusion.
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| How is flail chest treated? | O2 as needed to maintain O2 sats, analgesia. Stabilize flail segment w/positive pressure ventilation (CPAP, BIPAP), or intubation and mechanical ventilation. Treat assoc. injuries. Surgical fixation.
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| Blood rapidly collects in pericardial sac, compresses myocardium b/c the pericardium doesn't stretch, and prevents ventricles from filling. | cardiac tamponade
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| What are the CM of cardiac tamponade? | Muffled, distant heart sounds, hypotension, neck vein distention, increased central venous pressure.
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| What is the treatment for cardiac tamponade? | Medical emergency; pericardiocentesis w/surgical repair as appropriate.
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| How should the tubing for the chest tube drainage system be kept? | Loosely coiled below chest level. Tubing should drop straight from bed or chair to drainage unit. Do not let it be compressed.
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| What should the nurse observe for with the chest drainage system? | For air fluctuations (tidaling) and bubbling in the water-seal chamber.
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| With the chest drainage system, if tidaling (rising w/inspiration & falling w/expiration in the spontaneously breathing pt) is not observed, what could be some of the reasons for this? | The drainage system is blocked, the lungs are reexpanded, or the system is attached to suction.
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| With the chest drainage system what does it mean if there is a lot of bubbling occurring? | There may be an air leak in the drainage system or a leak from the pt (bronchopleural leak).
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| What would you do to check if there is a leak in the chest drainage system? | If the chest tube is connected to suction, disconnect from wall suction to check for tidaling, suspect a system leak if bubbling continues.
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| With a chest drainage system, what should you never do and why? | Never elevate the drainage system to the level of the pts chest b/c this will cause fluid to drain back into the lungs. Secure the unit to the drainage stand. Change the unit if the collection chamber is full. Don't try to empty it.
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| What should you do if you ever find the drainage container overturned and the water seal disrupted? | Return it to an upright position and encourage the pt to take a few deep breaths, followed by forced exhalations and cough maneuvers.
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| A reduction of platelets below 150000. | Thrombocytopenia
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| What is a risk when using heparin? | developing heparin induced thrombocytopenia (HIT)
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| When should HIT be expected? | Usually 5-10 days after the onset of therapy, and if the platelet count falls by more than 50% or falls to below 150000.
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| What is the major clinical problem with HIT? | venous thrombosis or arterial thrombosis; deep vein thromboses and pulmonary emboli most commonly result as a complication of the thromboses.
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| What are the CM of HIT? | Bleeding, usually mucosal (epitaxis & gingival bleeding)or cutaneous (petechiaie, purpura, or superficial ecchymoses, prolonged bleeding after venipuncture or IM injections; blood loss - weakness, fainting, dizzy, tachy, hypotension, abd pain
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| What should be done to treat HIT? | Stop the heparin. Anticoagulate w/lepirudin, argatroban, fondaparinux, or warfarin (only started when platelet count has reached 150000.
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| In HIT, what can be done if the clotting is too severe? | Plasmapharesis to clear the platelet aggregating IgG from the blood, protamine sulfate to interrupt circulating heparin, thrombolytic agents for thromboembolic events, surgery to remove clots.
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| Would you do platelet transfusions with HIT? | No, they are not effective because they may enhance thromboembolic events.
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| Are prepared from whole blood by sedimentation or centrifugation. One unit contains 250-350 mL. | packed RBCs
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| How long can packed RBCs be stored? | Up to 35 days depending on processing.
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| When would packed RBCs be used? | Severe or symptomatic anemia, acute blood loss.
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| If a patient has had a previous reaction to blood transfusions what could be used and why? | Leukoreduced packed RBCs; leukocyte depletion by filtration, washing, or freezing frequently used. Decreases hemolytic febrile or mild allergic reactions in patients who receive frequent transfusions.
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| Prepared from fresh whole blood. | platelets
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| When would a platelet transfusion be appropriate? | Bleeding caused by thrombocytopenia; may be contraindicated in thrombotic thrombocytopenic pupura and HIT.
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| Are prepared from RBCs using glycerol for protection and frozen. Can be stored for 10 yrs. | frozen RBCs
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| Liquid portion of whole blood is separated from cells and frozen. Is rich in clotting factors by contains no platelets. | fresh frozen plasma (FFP)
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| When would FFP be used? | Bleeding caused by deficiency in clotting factors (e.g. DIC, hemorrhage, massive transfusion, liver disease, Vit K deficiency, excess warfarin.
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| Prepared from plasma. Can be stored for 5 yrs. Available in 5% or 25% solution. | albumin
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| When would a transfusion of albumin be used? | hypovolemic shock, hypoalbuminemia
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| Prepared from fresh frozen plasma. Can be stored for 1 yr. Once thawed must be used within 5 days. | cryoprecipitate & commercial concentrates
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| When would cryoprecipitates be used? | Replacement of clotting factors, especially factor VIII, von Willebrand factor, and fibrinogen
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| With blood transfusions, what is a UAP allowed to do? | Obtain blood products from the blood bank as directed by RN. Take vitals before the transfusion & after the first 15 mins.
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| What is the LPN able to do during blood transfusions? | Assist w/checking pt ID & blood product ID data & monitor blood transfusion rate (per facility).
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| What is the role of the RN during blood transfusions? | Ensure proper size IV line (prefer 18g or higher), dbl check pt ID & blood product ID w/other RN, adjust infusion rate, evaluate for therapeutic effect (inc BP, improved pt color, dec bleeding), monitor for s/s of circulatory overload (SOB)
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| This can occur w/infusion of ABO incompatible whole blood, RBCs, or components containing >= 10 mL of RBCs. Antibodies in the recipient's plasma attach to antigens on transfused RBCs, causing RBC destruction. | acute hemolytic reaction
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| What are the CM of acute hemolytic reactions? | Reactions usually develop in first 15 min. Chills, fever, low back pain, flushing, tachycardia, dyspnea, tachypnea, hypotension, vascular collapse, hemoglobinuria, acute jaundice, dark urine, bleeding, AKI, shock, cardiac arrest, DIC, death
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| How do you manage acute hemolytic reactions? | Treat shock & DIC if present. Draw blood samples for testing. Maintain BP w/IV colloid solutions, give diuretics, monitor UO, dialysis if renal failure occurs, DO NOT TRANSFUSE add'l RBC til blood bank does new crossmatched units.
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| What are some ways to prevent acute hemolytic reactions? | Meticulously verify and document pt ID from sample collection to component infusion (visually compare label on sample collection & blood component w/pt ID).
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| This can occur due to a sensitization to donor WBCs (most common), platelets, or plasma proteins. | febrile, nonhemolytic reaction
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| What are the CM of febrile nonhemolytic reactions? | sudden chills, rigors, and fever (rise in temp of >1 C, headache, flushing, anxiety, vomiting, muscle pain
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| How should febrile nonhemolytic reactions be managed? | Give antipyretics as prescribed (acetaminophen). Avoid ASA in thromobcytopenic pts. DO NOT RESTART TRANSFUSION unless physician orders.
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| What are some ways to prevent febrile nonhemolytic reactions? | Consider lukocyte reducted blood products (filtered, washed, or frozen) for pts w/a history of 2 or more reactions. Give acetaminophen or diphenhydramine (Benadryl) 30 min before transfusion.
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| What is the most common reaction to transfusions? | febrile nonhemolytic reactions
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| This reaction can occur when replacement of RBCs or blood exceeds the total blood volume w/i 24 hr. RBC transfusions do not contain clotting factors, albumin, and platelets. | Massive blood transfusion reaction
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| What are the CM of massive blood transfusion reactions? | Hypothermia & cardiac dysrhythmias; citrate toxicity & hypocalcemia manifest as muscle tremors & ECG changes; hyperkalemia manifest as muscle weakness, diarrhea, paresthesias, paralysis of cardiac or resp muscles, & cardiac arrest.
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| When patients receive massive transfusions of blood products, what should the nurse monitor? | clotting status and electrolyte levels
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| What are some ways to prevent massive blood transfusion reactions? | Use blood warming equipment; infusion of 10% calcium gluconate (10mL w/every 1L of citrated blood).
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| This can occur as early as 3 days or as late as several month, but usually 5-10 days postransfusion. | delayed hemolytic reaction
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| What are the CM of delayed hemolytic reactions? | fever, mild jaundice, decreased Hgb
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| What are the primary causes of HF? | CAD (including MI), HTN, Rheumatic heart disease, congenital heart defects, pulmonary HTN, cardiomyopathy, hyperthyroidism, valve disorders, myocarditis
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| How can anemia cause HF? | Dec. O2 carrying capacity of the blood stimulate increase in CO to meet tissue demands, lead to inc. cardiac workload & inc. in size of LV.
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| How can nutritional deficiencies or hypervolemia cause HF? | Inc. preload causes volume overload on the RV.
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| What are the CM of right sided HF (Cor pulmonale)? | RV heaves, murmurs, JVD, edema (pedal, scrotum, sacrum), weight gain, inc. HR, ascites, anasarca (massive general body edema), hepatomegaly (liver enlargement)
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| What are the symptoms of right sided HF (Cor pulmonale)? | fatigue, anxiety, depression, dependent, bilateral edema, right upper quadrant pain, anorexia/GI bloating, nausea
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| What are the CM of left sided HF? | LV heaves, pulsus alternans (alternating pulses: strong, weak), PMI displaced (LV hypertrophy), dec. PaO2, slight Inc. PaCO2 (poor O2 exchange), crackles, S3 & S4 sounds, pleural effusion, change in LOC, restlessness, confusion
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| What are the symptoms of left sided HF? | weakness, fatigue, anxiety, depression, dyspnea, shallow resp. up to 32-40 min, paroxysmal nocturnal dyspnea, orthopnea (SOB in recumbent pos), dry, hacking cough, nocturia, frothy pink tinge sputum (adv. pulm. edema)
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| What lab is routinely checked for diagnosis of HF? | BNP
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| What are some drugs used to treat HF? | diuretics (Loop & thiazide, K sparing), ACEI, ARBs, vasodilators, B-adrenergic blockers, B-adrenergic agonists, Phosphodiesterase Inhibitors, digitalis glycoside, morphine, antidysrhythmics, anticoagulants
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| What is the mechanism of action for diuretics? | Dec. fluid volume, dec. preload, dec. pulonary venous pressure, relieve symptoms of HF (e.g. edema)
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| What are some examples of Loop diuretics? | furosemide (Lasix), bumetanide (Bumex)
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| What are some examples of thiazide diuretics? | hydrochlorothiazide (HCTZ), metolazone (Zaroxolyn)
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| What are some examples of K sparing diuretics? | spironolactone (Aldactone), eplerenone (Inspra)
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| What is the mechanism of action for ACE inhibitors and ARBs? | dilate venules & arterioles, improve renal blood flow, dec. fluid volume, relieve symptoms fo HF, promote reverse remodeling, dec. morbidity & mortality
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| Examples of ACE inhibitors. | captopril (Capoten), benazepril (Lotensin), enalapril (Vasotec)
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| Examples of ARBs. | losartan (Cozar), valsartan (Diovan)
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| What is the MOA for vasodilators? | Reduce cardiac afterload, leading to inc. CO; dilate the arterioles of kidneys lead to inc. renal perf & fluid loss, dec. BP, dec. preload, relieve symptoms of HF (dyspnea)
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| Examples of vasodilators. | hydralazine (Apresoline), isosorbide dinitrate hydralazine (BiDil), nitrates (nitroglycerin-NitroBid, isosorbide dinitrate-Isordil), nesiritide (Natrecor), nitroprusside (Nipride)
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| What is the MOA for B-adrenergic blockers? | Promote reverse remodeling, dec. afterload, inhibt SNS, dec. morbidity & mortality
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| Examples of B-adrenergic blockers. | metoprolol (Toprol), bisoprolol (Zebeta), carvedilol (Coreg)
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| What are positive inotropes? | B-adrenergic agonists, phophodiesterase inhibitor, digitalis glycoside
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| What is the MOA for positive inotropes? | Inc. contractility (pos. inotropic effect), inc. CO, inc. HR (pos chronotropic effect), produce mild vasodilation, inc. SV & CO, promote vasodilation
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| Examples of positive inotropes. | dopamine (Intropin), dobutamine (Dobutrex), milrinone (Primacor), digoxin (Lanoxin) epinephrine, norepinephrine (Levophed)
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| What is the MOA for morphine? | Dec. anxiety, dec. preloand and afterload
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| What is the MOA for antidysrhythmics? | Prevent or treat dysrhythmias.
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| What is the MOA for anticoagulants? | Prevent thromboembolism; recommended for pts w/an ejection fraction <20% and/or atrial fib.
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| Represents time for the passage of the electrical impulse through the atrium causing atrial depolarization (contraction). Should be upright. | P wave
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| What is the normal duration for the P wave? | 0.06-0.12 sec
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| Measured from beginning of P wave to beginning of QRS complex. Represents time taken for impulse to spread through the atria, AV node, and bundle of His, bundle branches, & Purkinje fibers to a point immed preceding vent. contraction. | PR interval (PRI)
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| What is the normal duration for the PRI? | 0.12-0.20 sec
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| Q wave: first neg. deflection, after the P wave, short & narrow, not present in several leads; R wave: first pos. deflection; S wave: first neg. deflection after the R wave | QRS complex
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| What is the normal duration of the QRS complex? | Q wave is <0.03, while the R and S waves are not usually measured
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| Measured from beginning to end of QRS complex. Represents time taken for depolarization (contraction) of both ventricles (systole). | QRS interval
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| What is the normal duration of the QRS interval? | <0.12 sec
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| Represents time for ventricular repolarization. Should be upright. | T wave
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| Measured from the S wave of the QRS complex to the beginning of the T wave. Represents the time b/t ventricular depolarization & repolarization (diastole). Should be isoelectric (flat). | ST segment
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| What is the normal duration of the ST segment? | 0.12 sec
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| What is the normal duration of the T wave? | 0.16 sec
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| Measured from beginning of QRS complex to end of T wave. Represents time taken for entire electrical depolarization and repolarization of the ventricles. | QT interval
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| What is the normal duration of the QT interval? | 0.34-0.43 sec
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| What would cause disturbances (e.g. elevation, depression) with the ST segment? | ischemia, injury, or infarction
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| What would cause variations in the QRS interval? | Disturbance in conduction in bundle branches or in ventricles.
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| What would cause a T wave to become tall, peaked, or inverted? | Caused by electrolyte imbalances, ischemia, or infarction
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| What could cause variations in the P wave? | disturbance in conduction within the atria
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| What would cause variations in the PRI? | Disturbance in conduction usually in AV node, bundle of His, or bundle branches but can be in atria as well
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| What does one large square on a rhythm strip represent? | 0.2 sec; 5 mm (horizontally); 0.5 mV (vertically)
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| What does one of the smaller boxes within the large box on a rhythm strip represent? | 0.04 sec; 1 mm (horizontally); 0.1 mV (vertically)
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| The SA node produces a HR of? | 60-100 bpm
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| The AV node produces a HR of? | 40-60 bpm
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| The bundle of His and Purkinje fibers produce a HR of? | 20-40 bpm
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| What are some cardiac conditions that could cause dysrhythmias? | accessory pathways, cardiomyopathy, conduction defects, HF, myocardial ischemia, MI, valve disease
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| What conditions can cause dysrhythmias? | acid base imbalances, alcohol, caffeine, tobacco, connective tissue disorders, drugs, electric shock, electrolyte imbalances, emotional crisis, hypoxia, metabolic conditions, sepsis, shock, toxins, near drowning, herbal supp
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| Assessing heart rhythms: Step 1 | Look for the P wave, is it upright or inverted? Is there one for every QRS complex or more than one? Are atrial fibrillatory or flutter waves present?
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| Assessing heart rhythms: Step 2 | Evaluate the atrial rhythm. Is it regular or irregular?
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| Assessing heart rhythms: Step 3 | Calculate the atrial rate.
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| Assessing heart rhythms: Step 4 | Measure the duration of the PRI. Is it normal duration or prolonged?
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| Assessing heart rhythms: Step 5 | Evaluate the ventricular rhythm. Is it regular or irregular?
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| Assessing heart rhythms: Step 6 | Calculate the ventricular rate.
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| Assessing heart rhythms: Step 7 | Measure the duration of the QRS complex. Is it normal duration or prolonged?
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| Assessing heart rhythms: Step 8 | Assess the ST segment. Is it isoelectric (flat), elevated, or depressed?
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| Assessing heart rhythms: Step 9 | Measure the duration of the QT interval. Is it normal duration or prolonged?
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| Assessing heart rhythms: Step 10 | Note the T wave. Is it upright or inverted?
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| What are the CM of dysrhythmias (same for dec. CO)? | dec/ inc BP, irreg rt/ rthm, tachy brady dec O2 sats chest neck shoulder back jaw or arm pain dizzy, syncope, dyspnea, restless, anxiety, dec. LOC, confusion, numbness, tingling, weak & fatigue, cold clammy skin, dim pulses, diaphor, pallor, palps, N/V
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| What are the initial interventions for a pt with dysrhythmias? | Ensure ABCs, O2, vitals (inc O2 sats), 12 lead ECG, continuous ECG monitoring, identify underlying rate & rhythm, identify dysrhythmia, IV access, baseline labs (e.g. CBC, electrolytes)
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| What would the nurse monitor with dysrhythmia pts? | Monitor vitals, LOC, O2 sats, & cardiac rhythm; anticipate need for antidysrhythmia drugs & analgesics; prepare to initiate adv cardiac life support (CPR, defib, transcutaneious pacing)
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| Rhythm: 60-100 bpm & reg, P wave normal; PRI normal; QRS complex normal | normal sinus rhythm
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| Rhythm: <60 bpm & reg, P wave normal; PRI normal; QRS complex normal | sinus bradycardia
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| Rhythm: 101-200 bpm & reg, P wave normal; PRI normal; QRS complex normal (usually) | sinus tachycardia
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| Rhythm: Atrial 200-350 bpm/reg, Ventricular > or <100 bpm/irreg, or reg, F waves (saw tooth pattern), more F waves than QRS complexes, PRI not measureable, QRS complex normal (usually) | atrial flutter
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| Rhythm: Atrial 350-600 bpm/irreg, Ventricular > or <100 bpm/irreg, fibrillatory (f) waves, PRI not measureable, QRS complex normal (usually) | atrial fibrillation
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| Rhythm: Normal rate/rhythm, normal P wave, PRI >0.20 sec, QRS complex normal | first degree AV block
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| Rhythm: Atrial normal/reg, ventricular slower/irreg, P wave normal, PRI progressive lengthening, normal QRS width w/pattern of one nonconducted (blocked) QRS complex | Second degree AV block: Type 1 (Mobitz 1, Wenckebach heart block)
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| Rhythm: Atrial usually normal/reg, ventricular slower/reg or irreg, more P waves than QRS complexes, PRI normal or prolonged, widened QRS, preceded by >=2 P waves w/nonconducted (blocked) QRS complex | Second degree AV block: Type II (Mobitz II heart block)
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| Rhythm: Atrial reg but may appear irreg due to P waves hidden in QRS complexes, ventricular 20-60 bpm/reg, P wave normal but no connection w/QRS complex, PRI variable, QRS complex normal or widened, no relationship w/P waves | Third degree AV block (complete heart block)
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| Rhythm: underlying rhythm can be any rate, reg/irreg rhythm; these occur at variable rates; P wave not usually visible, hidden; PRI not measurable; QRS complex wide & distorted | Premature ventricular contraction (PVC)
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| Rhythm: 150-250 bpm & reg/irreg; P wave not usually visible; PRI not measurable, QRS complex wide & distorted | Ventricular tachycardia
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| Rhythm: Rate & rhythm not measurable & irreg; P wave absent; PRI not measurable; QRS complex not measurable | Ventricular fibrillation
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| What is the primary goal in treatment of Aflutter & Afib? | To slow the ventricular response by increasing AV block.
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| What drugs are used with Aflutter? | CCBs & BBs control ventricular rate; antidysrhythmia drugs used to convert to sinus rhythm such as ibutilide (Corvert); amiodarone, flecainide (Tambocor), dronedarone (Multaq) to maintain sinus rhythm
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| What procedure may be performed to convert atrial flutter to sinus rhythm in an emergency (i.e. when pt is clinically unstable)? | electrical cardioversion; must anticoagulate first
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| What are Afib and Aflutter patients at risk for and how is it treated? | Risk of thrombus formation due to stasis of blood in the atria which could lead to stroke or PE. Must be anticoagulated usually with warfarin (Coumadin).
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| What drugs are used for Afib? | CCBs (diltiazem); BBs (metoprolol); dronedarone, and digoxin (Lanoxin) for rate control
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| What is the treatment of choice for Aflutter? Describe. | radiofrequency catheter ablation; involves placing a catheter in the right atrium, w/use of low voltage, high frequency form of electrical energy, the tissue is ablated (destroyed), the dysrhythmia is ended, NSR restored
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| What labs are routinely monitored for patients on anticoagulants? | PT and INR
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| What are some different anticoagulants used and which is the drug of choice? | warfarin (Coumadin), dabigatran (Pradaxa), apixaban (Eliquis), rivaroxaban (Xarelto); warfarin is the drug of choice
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| PT | 11-13 sec
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| INR | 0.8-1.2
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| PTT | 25-35 sec
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| For drug refractory Afib or those pts who do not respond to electrical cardioversion, what can be used? | radiofrequency catheter ablation (similar to Aflutter) and the Maze procedure
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| What is the Maze procedure? | A surgical intervention that stops Afib by interrupting the ectopic electrical signals that are responsible for the dysrhythmia. Incisions are made in both atria & cryoablation (cold therapy) stops formation & conduction of these signals & restore NSR.
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| This type of heart block has a PRI of 0.24; everything else is normal and regular. | First degree AV block
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| This heart block has a PRI of 0.20, then 0.24, then 0.30 and then a QRS drops and cycles back again. | Second degree AV block Type 1 (Mobitz 1 or Wenckebach)
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| This heart block has a constant PRI of 0.30 and variable blocked QRS complexes. | Second degree AV block Type 2 (Mobitz 2)
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| This heart block has no impulses from the atria conducted to the ventricles. The atria are stimulated & contract independently of the ventricles. Ventricular rhythm is an escape rhythm & ectopic pacemaker above or below the bifurcation of bundle of His | Third degree AV block
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| What is the treatment for Second degree Type II blocks and Third degree AV blocks? | pacemaker
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| What drugs are used to increase HR and support BP until temporary pacing can be started? | atropine, dopamine, and epinephrine
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| PVCs that arise from different foci appear different in shape from each other and are called? | multifocal PVCs
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| PVCs that have the same shape are called? | unifocal PVCs
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| When every other beat is a PVC, the rhythm is called? | ventricular bigeminy
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| When every third beat is a PVC, it is called? | ventricular trigeminy
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| Two consecutive PVCs are called? | couplet
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| Three or more PVCs consecutively are called? | ventricular tachycardia
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| What can cause PVCs? | caffeine, alcohol, nicotine, aminophylline, epinephrine, isoproterenol, and digoxin; also associated w/electrolyte imbalances, hypoxia, fever, exercise, & emotional states; associated w/MI, mitral valve prolapse, HF, & CAD
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| What is the treatment for PVCs? | Treat the underlying cause of the PVC (e.g. O2 therapy for hypoxia, electrolyte replacement). Assess pts hemodynamic status to determine if drug therapy is needed. Drugs include BBs, procainamide (Pronestyl), amiodarone
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| "Twisting of the points"; is a polymorphic Vtach associated w/a prolonged QT interval of the underlying rhythm. | Torsades de pointes
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| What is Torsades treated with? | Mg
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| How is a clinically stable (pulse present)pt w/Vtach, that has preserved left ventricular function treated? | IV procainamide, sotalol, or amiodarone
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| What is the treatment for a pt that has unstable (w/o a pulse) Vtach? | CPR, rapid defibrillation first lines of treatment; then administer vasopressors (epinephrine) and antidysrhythmics (amiodarone, lidocaine)
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| On an ECG it is characterized by irregular waveforms of varying shapes and amplitude. The ventricle is simply "quivering" w/no effective contraction & no CO occurs. Is a lethal dysrhthmia. | Ventricular fibrillation
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| How is Vfib treated? | same as Vtach; CPR, defib, amiodarone, lidocaine
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| Antidysrhythmia drugs | Sodium channel blockers; B-adrenergic blockers; Potassium channel blockers; Calcium channel blockers; other - adenosine (Adenocard), digoxin (Lanoxin), dronedarone (Multaq), Mg (for Torsades
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| Sodium channel blockers | disopyramide (Norpace)0,, procainamide (Pronestyl), quinidine (Quinora), mexiletine (Mexitil), phenytoin (Dilantin), flecainide (Tambocor), propafenone (Rythmol)
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| B-adrenergic blockers | esmolol (Brevibloc), metoprolol (Lopressor), propanolol (Inderal)
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| Potassium channel blockers | amiodarone (Cordarone), bretylium (Bretylol), dofetilide (Tikosyn), ibutilide (Corvert), sotalol (Betapace)
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| Calcium channel blockers | diltiazem (Cardizem), verapamil (Calan)
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| What are the differences between cardioversion and defibrillation? | Cardioversion is for stable pts, at a lower volt setting and is synched with the R wave. Defibrillation is for unstable (w/o a pulse) pts at a higher volt setting and is not synced just shock at any time.
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| This sense's the heart's electrical activity and fire only when the HR drops below a preset rate. | demand pacemakers
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| What are the 2 distinct features of demand pacemakers? | A sensing device that inhibits the pacemaker when the HR is adequate. A pacing device that triggers the pacemaker when no QRS complexes occur within a preset time.
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| What are permanent pacemakers? | Implanted totally within the body. The power source is placed subcutaneously over the pectoral muscle on pts nondom side. Pacing leads placed transvenously to rt atrium & 1 or both ventricles & attached to power source.
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| This pacemaker has the power source outside the body. | temporary pacemakers
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| What are the three types of temporary pacemakers? | transvenous pacemaker, epicardial pacing, transcutaneous pacemaker
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| Consists of a lead(s) that are threaded to the rt atrium & or rt ventricle & attached to the external power source. Usually inserted in ERs & critical care units in emergent situations. | transvenous pacemakers
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| Involves attaching an atrial & ventricular pacing lead to the epicardium during heart surgery. The leads are passed through the chest wall & attached to the external power source. Placed prophylactically. | epicardial pacemaker
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| Provide adequate HR and rhythm to the pt in an emergency situation. Placement is noninvasive and temporary til transvenous pacemaker is inserted. | transcutaneous pacemaker
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| What are some indications for permanent pacemakers? | acquired AV block, 2nd & 3rd degree AV block, Afib w/slow ventricular response, bundle branch block, cardiomyopathy, HF, SA node dysfunction, tachydysrhythmias (Vtach)
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| What are some indications for temporary pacemakers? | Maintenance of adequate HR & rhythm during surgery & postop, during cardiac cath or coronary angioplasty, drugs that cause brady.; before a perm. pacemkr; prophylaxis after open heart surgery; acute MI, electrophysiologic studies w/brady/tachydysrhythmias
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| What are some complications of pacemakers? | infection; hematoma formation at insert. site; pneumothorax; failure to sense or capture; peforation of the atrial or ventricular septum by the pacing lead; & appearance of "end of life" battery power on testing the pacemaker.
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| What measure can prevent or assess these complications with pacemakers? | prophylactic IV antibiotic therapy before & after insertion; postinsertion chest x ray to check lead placement & to rule out a pneumo; careful observation of insertion site & continuous ECG monitoring of pts rhythm
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| What should the nurse educate the pt about after the pacemaker has been inserted? | Pt can be out of bed once stable; limit arm & shoulder activity on the operative side to prevent dislodging the pacing leads; observe insertion site for signs of bleeding & incision intact; note temp change or pain & treat as needed.
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| An infection of the endocardial (innermost) layer of the heart. | infective endocarditis
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||||
| What can cause infective endocarditis (IE)? | Most common causes from Staphylococcus aureus & Streptococcus viridans (bacterial); fungi & viruses
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|
||||
| What are vegetations in IE? | The primary lesions of IE, consist of fibrin, leukocytes, platelets, & microbes that stick to the valve surface or endocardium.
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||||
| What can occur if one of these vegetations breaks off into the circulation? | embolus
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||||
| A left sided heart vegetation that breaks off can move where? | Various organ (brain, kidneys, spleen); extremities; anywhere
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|
||||
| A right sided heart vegetation that breaks off can move where? | into the lungs causing a PE
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|
||||
| What are the CM of IE? | Low grade fever, chills, weakness, malaise, fatigue, anorexia, arthralgias, myalgias, back pain, abdominal discomfort, weight loss, headache, & clubbing of fingers
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||||
| What are some vascular manifestations of IE? | splinter hemorrhages (black longitudinal streaks) in the nail beds; petechiae in conjunctiva, lips, buccal mucosa, palate, & over ankles, feet, AC, & pop areas. Osler's nodes, Janeway lesions, Roth spots
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||||
| These are painful, tender, red or purple, pea size lesions found on fingertips or toes that may occur with IE. | Osler's nodes
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|
||||
| These are flat, painless, small, red spots that may be seen on the palms and soles that may occur with IE. | Janeway's lesions
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|
||||
| These are retinal lesions that may occur with IE. | Roth's spots
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|
||||
| What labs would be elevated with IE? | erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)
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|
||||
| erythrocyte sedimentation rate (ESR) | 0-20 mm/hr - men; 0-29 mm/hr - women
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||||
| CRP | 0-10 mg/L
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|
||||
| A condition caused by inflammation of the pericardial sac (the pericardium). | pericarditis
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|
||||
| What are some common infectious causes of pericarditis? | Viral: Coxsackie A & B virus, echovirus, adenovirus, mumps, hepatitis, Epstein Barr, varicella zoster, HIV; Bacterial: pneumococci, staph, strep, Neisseria gonorrhea, Legionella, TB, septicemia.; Fungal: histoplasma, Candida; toxoplasmosis, Lyme disease
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| What are some noninfectious causes of pericarditis? | uremia, acute MI, neoplasms: lung cancer, leukemia, Hodgkin's lymphoma, non-Hodgkins lymphoma; Trauma: thoracic surgery, pacemaker insert., cardiac diagnostic proc.; radiation; dissecting aortic aneurysm; myxedema
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|
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| What are the CM of pericarditis? | Progressive, frequently severe, sharp chest pain (worse w/inspiration & lying supine). Pain may radiate to neck, arms, left shoulder, dyspnea, fever, anxiety
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| What is the hallmark finding in acute pericarditis? | pericardial friction rub; a scratching, grating, high-pitched sound believed to result from friction b/t the roughened pericardial & epicardial surfaces
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||||
| Where is a pericardial friction rub best heard? | Stethoscope placed at the lower left sternal border of the chest w/the pt leaning forward.
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|
||||
| How can you distinguish b/t a pericardial friction rub and a pleural friction rub? | Ask pt to hold their breath, if you still hear the rub then it's cardiac. May require frequent attempts b/c pericardial friction rubs are intermittent & short lived.
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||||
| How can you relieve some of the pain with pericarditis? | Have the pt sit up and lean forward.
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||||
| What are two major complications that can arise from pericarditis? | pericardial effusions & cardiac tamponade
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|
||||
| A build up of fluid in the pericardium. It can occur rapidly (chest trauma) or slowly (tuberculosis pericarditis). Heart sounds are generally distant & muffled, but BP usually maintained. | pericardial effusions
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|
||||
| This develops as the pericardial effusion increases in volume resulting in compression of the heart. The speed of the fluid accumulation affects the severity of CM. | cardiac tamponade
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|
||||
| Examples of acute cardiac tamponade. | rupture of heart, trauma
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|
||||
| Examples of subacute cardiac tamponade. | secondary to renal failure, malignancy
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|
||||
| What are some CM of cardiac tamponade? | May report chest pain, confused, anxious, restless. As compression increases CO decreases, muffled heart sounds, narrow pulse pressure, tachypnea/tachycardia, JVD, & pulsus paradoxus is present
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||||
| What is pulsus paradoxus? | A decrease in systolic BP during inspiration that is exaggerated in cardiac tamponade.
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|
||||
| How is pericarditis managed? | Treat underlying problem. Bed rest, Antibiotics for bacterial; NSAIDs (ASA, ibuprofen) control pain & inflammation; corticosteroids (generally reserved for pericarditis secondary to SLE)
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|
||||
| What antiinflammatory drug typically used for gout can be used for pts who have recurrent pericarditis? | colchicine (Colsalide)
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|
||||
| When is a pericardiocentesis usually performed? | For pericardial effusions w/acute cardiac tamponade, purulent pericarditis, and suspected neoplasm.
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|
||||
| What diagnostics can be done for pericarditis? | Histyory & physical (peri. friction rub, pulsus paradoxus); CRP; ESR; WBC ct; ECG; chest xray; echocardiogram; computed tomography; MRI; pericardiocentesis; pericardial window; pericardial biopsy
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||||
| What are the CM of mitral valve stenosis? | dyspnea on exertion, hemoptysis, fatigue, Afib on ECG, palpitations, stroke, loud accentuated S1; low pitche diastolic murmur
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||||
| What are the CM of mitral valve regurgitation? | Acute: generally poorly tolerated, new systolic murmur w/ pulmonary edema & cardiogenic shock developing rapidly; Chronic: weakness, fatigue, exert. dyspnea, palpitation, S3 gallop, holosystolic murmur
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||||
| What are the CM of mitral valve prolapse? | palpitations, dyspnea, chest pain, activity intolerance, syncope, or holosystolic murmur
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|
||||
| What are the CM of aortic valve stenosis? | Angina, syncope, dyspnea on exertion, HF, normal or soft S1, diminished or absent S2, systolic murmur, prominent S4
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|
||||
| What are the CM of aortic valve regurgitation? | Acute: abrupt onset of profound dyspnea, chest pain, lt vent. failure & cardio. shock; Chronic: fatigue, exert. dyspnea, orthopnea, water-hammer pulse, heaving precordial impulse, dim/absent S1 S3 or S4, soft high pitch dias. murmur Austin Flint murmur
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| What are the CM of tricuspid and pulmonic stenosis? | Tricuspid: Per. edema, ascites, hepatomegaly, diastoli low pitch murmur w/increased intensity during insipration; Pulmonic: fatigue, loud midsystolic murmur
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||||
| What is a stenotic valve? | constricted or narrow; the valve is not opening completely to move blood forward
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|
||||
| What is a regurgitant valve? | incompetent or insufficient; the valve is not closing properly resulting in backward flow of blood
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|
||||
| What diagnostics would be used to diagnose valvular heart disease? | History & physical, chest xray, CBC, ECG, echo (Doppler & transesophageal), cardiac catherization
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|
||||
| What drugs are used to manage HF? | nitrates (nitroglycerin-Nitrol), diuretics (furosemide-Lasix), dec. preload; ACEI (captopril-Capoten) reduce afterload; BBs (metoprolol-Lopressor) & aldosterone antag. (spironolactone-Aldactone); antidysrhthmics (amiodarone), anticoagulants
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|
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