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365 Cards in this Set
- Front
- Back
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Inability of the left ventricle to pump enough blood. A reduction in EF?
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Systolic Heart Failure
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Left ventricle is unable to fill because it can't relax. The wall is stiff and may be due to ventricular hypertrophy?
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Diastolic Heart Failure
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Caused by systemic hypertension, myocardial infarctions or structural heart changes?
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Heart Failure
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Caused by left sided heart failure. Pulmonary hypertension either alone or as a result of hypoxia?
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Right Sided Heart Failure
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Increased demands on the body?
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High Output Failure
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HR times SV equals?
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Cardiac Output
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The amount of blood pumped by a ventricle with each contraction?
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Stoke Volume
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The amount of myocardial stretch just before systole?
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Preload
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The amount of resistance to the ejection of blood from ventricles?
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Afterload
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The force of contraction related to the number and status of myocardial cells?
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Contractility
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What are the two main compensatory mechanisms of heart failure?
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The sympathetic and renin-angiotensin system.
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Hypoxia from decreased cardiac output increases catecholamines and norepinephrine. Heart rate and BP increase. O2 demand and afterload increase vasoconstriction and remodeling?
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The sympathetic nervous system compensatory mechanism in heart failure.
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Decreased blood flow to the kidneys. Increased vasoconstriction as renin is increased. Aldosterone is increased. Fluid retention. Ventricular remodeling?
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The Renin-Angiotensin System compensatory mechanism in heart failure.
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Increases ventricular remodeling and endothelincytokines?
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Immune response hormones to heart failure.
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Promotes water and sodium loss, released from overdistended left ventricle?
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The BNP.
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Increases fluid retention?
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Vasopressin from the brain.
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Ventricular remodeling, walls thicken, chambers enlarge, increases O2 demands on the heart?
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Myocardial hypertrophy. A result of neuro-hormonal stimuli.
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Pulmonary congestion when left ventricle cannot pump well. DOE, orthopnea, paroxymal nocturnal dyspnea, oliguria due to poor perfusion, weak pulses and cool extremities?
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Left Sided Heart Failure
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Fatigue, weakness, dizziness, confusion caused by decreased blood flow to the brain, angina, irregular heart rate, tachycardia, pulses alternans, enlarged heart and S3 sound indicating left ventricular filling pressure?
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Left Sided Heart Failure
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Congestion of viscera and peripheral tissues due to right ventricle failure?
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Right Sided Heart Failure
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Jugular vein distention, dependent edema, hepatomegaly, ascites, weakness, anorexia, nausea and weight gain?
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Right Sided Heart Failure
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Normal EF?
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60% - 70%
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An EF level indicating the need for treatment?
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40%
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Renal and Hepatic functions, BNP, thyroid panel, iron, lytes, CA, MG, lipids, UA, cystatin C?
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Heart failure lab work
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Shows heart size, prescence of pulmonary abnormalities, congestion, effusion and edema?
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Chest X-ray
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Reveals cardiac rhythm and rate, ischemia and infarctions, hypertrophy, enlargement and electorlyte abnormalities?
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EKG
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Shows chamber size and function, wall thickness, thrombus, structural problems, and EF?
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Echocardiogram with doppler
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Radionuclide ventriculography nuclear medicine scan, can give more info on EF?
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MUGA
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Stress test if the patient has?
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Angina
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If the patient has chest pain and is a candidate for revascularization?
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Cardiac Cath.
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I&O, Daily weights, auscultate lung sounds, determine degree of JVD, assess dependent edema, and monitor VS?
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Nursing Management - Heart Failure
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What must the pt have once a year and what must the pt have every five years?
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Flu vaccine every year and pneumococcal every five years
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HF risk factors, no disease, no symptoms?
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Stage A heart failure
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Heart disease, no symptoms, asymptomtic left ventricular dysfunction, may be taking an ACE or a Beta-blocker?
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Stage B heart failure
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Prior or current heart failure symptoms, modify diet, may be on a diuretic, may need bi-ventricle pacing, avoid non-steriodal anti-inflammatory drugs, probably going to be on anticoagulation therapy?
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Stage C heart failure
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Advanced refractory heart failure symptoms with rest and minimal exertion, needing frequent intervention in an acute setting, try and prove cardiac performance, facilitate diuresis, stabilize?
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Stage D heart failure
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Cardiac resynchronization therapy?
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CRT
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For patients with class III-IV heart failure, Cardiomyopathy, bundle brance block causes dyssynchronous conduction and contration-wide QRS, increases cardiac output, may be combine with defibrillator?
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CRT
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Prils?
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ACE
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OLOL?
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Beta-blockers
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Used to reduce the effects of sodium and water retention, vasoconstriction and myocardial remodeling?
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ACE's, ARB's if ACE's not tolerated
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Used to reduce symptoms, improve clinical status, reduce mortality, must titrate up?
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Beta-blockers
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Start with a very low dose, increase if tolerated, monitor potassium and renal function, avoid fluid retention?
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ACE
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Hypotension (first dose effect), watch renal function, hyperkalemia, cough, angio-edema, rash, neutropenia?
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ACE adverse effects
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Increase density of B1 receptors, inhibits cardio toxicity of catecholamines, inhibits neuro hormonal activation, decreases HR?
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Beta-blocker
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Is an anti-ischemic, antihypertensive, antiarrythmic, antioxidant, and antiproliferant?
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Beta-blocker
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No physical evidence of fluid retention, no need of IV inotropic drugs, start an ACE and a diuretic first, no contraindications, you can be in the hospital or not?
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When to start a beta-blocker
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Beta-blockers
Starting Dose is 1.25 every 24hrs. Target dose is 10 every 24hrs? |
Bisoprolol
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Beta-blockers
Starting dose is 3.125 q 12hrs. Target dose is 25 q 12 hrs. |
Carvedilol
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Beta-blockers
Starting dose is 6.25 q 12hrs. Target dose is 75 q 12hrs. |
Metoprolol tartrate
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Beta-blockers
Starting dose is 12.5-25 q 24hrs. Target dose is 200 q 24hrs. |
Metoprolol succinnate
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Start low, increase slowly, increase the dose every 2 to 4 weeks?
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Beta-blockers
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Hypotension, fluid retension, worsening of heart failure, fatigue, bradycardia, and heart block?
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Adverse effects of Beta-blockers
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Asthma, AV block (unless you have a pacemaker), hypotension, bradycardia?
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Contraindications for Beta-blockers
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Diabetes is NOT a contraindication for?
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Beta-blocker
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Diuretics loop for FVE, thiazide for less FVE or in combo, aldosterone antagonists which play an increasing role in heart failure?
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Interventions that reduce preload
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Start with a variable dose and titrate, monitor potassium frequently, reduce dose when fluid retention is controlled, teach pt when and how to change dose, combined to overcome resistance and do not use alone?
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Loop diuretics\thiazides
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Recent or current symptoms despite ACE, diuretics, dig and beta-blocker?
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Spironolactone indications
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Recommended in advanced heart failure (C&D) in addition to ACE and diuretics, hypokalemic pt?
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Indication for Spironolactone
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Do not use if hyperkalemia, renal problems, monitor potassium frequently, should start an ACE first?
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Practical use for Spironolactone
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Start with 25mg q 24hrs. Potassium greater than 5.5, reduce to 25mg q 48hrs. Potassium low or stable, consider 50mg per day?
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Practical use for Spironolactone
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Increases the survival rate among black pt's with stage C-D HF after having tried ACE and Beta-blocker?
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Isordil and hydralzine (BiDil)
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Avoid or discontinue these medications that interfere with HF therapy?
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Anti-inflammatories and Calcium channel blockers
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These decrease cardiac contrility?
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Verapamil and diltiazem
nondihydopyridines-norvasc |
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Sodium restriction, fluid restriction and daily weights?
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Diet to reduce preload
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Used to increase contractility and reduce sodium absorption?
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Digoxin
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Recommended use of this drug only in pts who are symptomatic despite therapy with ACE inhibitors, Beta-blockers, and diuretics?
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Digoxin
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May be used to control rate in A-fib?
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Digoxin
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Monitor heart rate and electrolytes, toxicity includes anorexia, fatigue and changes in mental status?
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Digoxin
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Drug used in refractory HF?
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Inotropics (only in select pts)
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Drug used for ischemia, angina, and pulmonary congestion?
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Nitrates (only in select pts)
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Drug used when there is a contraindication to ACE?
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ARB (only in select pts)
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Anti-arrythmic drug?
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Amiodarone (only in select pts)
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Used when there is a high risk of embolism?
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Anti-coagulants (only in select pts)
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Used in pts with ischemia, only amlodipine?
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Calcium channel blocker (only in select pts)
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IV heart failure drugs are used only when?
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A pt has failed oral therapy
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Evidence of poor perfusion
Improves cardiac contractility Interferes with Beta-blockers Drug of choice if hypotensive, less vasodialating? |
IV Dobutamine
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Enhances calcium entry into the cells to increase contractility, pt must not be hypotensive, improves quality NOT quantity of life, very controversial?
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IV drug Primacor -milrinone - phosphodiesterase
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Human BNP causes loss of sodium and lowers PCWP, causes vasodilitation, decreases dyspnea, improves glomerular filtration, has increased mortality rate, medicare won't pay?
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IV drug Natrecor
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Inotropes, long term / intermittent
Antiarrhythmics (except amiodarone) Calcium antagonists (except amiodipine) Non-steroidal antiinflammatory drugs (NSAIDS) Tricyclic antidepressants Corticosteroids Lithium? |
Drugs to Avoid (may increase symptoms, mortality)
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Activity intolerance, fluid volume excess, anxiety, risk of impaired gas exchange, health maintenance?
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Nursing Dx
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Uses a three lead placement, can restore ventricular syncrony in pts with HF and conduction defects?
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Bi ventricle pacing
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Exam skin turgor and mucous membranes, assess excess of fluid overload?
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Nursing Management of HF
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BNP greater than 900, BUN greater than 43, SBP less than 115, Creatinine greater 2.2, and and elevated troponin?
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Factors that increase mortality in HF
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Pulmonary edema, restlessness and anxiety, cyanosis, weak rapid pulse, coughing with mucoid sputum?
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Acute HF
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Assess for early signs such as crackles in the lung bases, dyspnea at rest, disorientation and confusion?
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Intervention pulmonary edema
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Use a rapid acting diuretic such as lasix or bumex, oxygen, monitor, stict I&O?
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Intervention pulmonary edema
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Oxygen, morphine, diuretics, dobutamine, milrinone, and nesiritide?
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Pharmacological therapy of HF
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Occurs with moderate to prolonged exertion, is not getting worse and is relieved with nitro and rest?
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Stable angina
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Unpredictable, can occur at rest, increases in frequency, duration, and intensity, may or may not be relieved with nitro and rest, part of acute coronary syndromes, needs evaluated, ten to thrity percent MI in a year, no change in blood tests or EKG?
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Unstable angina
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An abnormal accumulation of lipids and fibrous tissue in the vessel wall?
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Athersclerosis
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Protrude into the lumen of the vessel, narrowing it and reducing blood flow?
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Atheromas or plaque
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Obstructs blood flow leading to MI or sudden death?
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Thrombus
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Hyperlipidemia, foam cells, plaque formation, inflammation, endothelial damage, plaque hemorage and thrombosis?
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Development of Atherosclerosis
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Increased levels are associated with the risk of CAD, TX with vitamins, serum marker for Atherosclerosis?
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Increased Homocysteine
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Bids to macrophages and promotes foam cells, a serum marker of Atherosclerosis?
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Lipoproteins or LDL
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Marker for systemic information, a major risk factor even with normal LDL, serum marker for Atherosclerosis?
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C reactive protein (CRP)
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Age, gender, family hx, and ethnicity?
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Non modifiable risk factors for Atherosclerosis
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Elevated serum cholesterol, smoking, htn, impaired glucose tolerance, obesity, inactivity and stress?
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Modifiable risk factors for Atherosclerosis
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The number 1 killer of women, pain may be in the shoulders, jaw, or a feeling of choking, not taken seriously, conflicting reports regarding hormones?
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Women health concerns regarding Atherosclerosis
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Exercise stress test may yeild false positives, cardiac cath may be the most reliable?
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Cardiac tests in women
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Includes stable angina and acute coronary syndromes?
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CAD
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Oxygen supply that is insufficient to meet the requirements of the myocardial muscle?
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Ischemia (CAD)
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Necrosis or cell death that occurs when severe ischemia is prolonged and irreversible damage to tissue results, detected with blood tests and EKG?
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Infarction (CAD)
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A feeling of strangling of the chest, temporary imbalance between the coronary arteries ability to supply oxygen and the cardiac muscles demand for oxygen, limited ischemia not causing damage?
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Stable angina pectoris
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Stopping pain is priority nursing concern?
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Tx of anginal pain
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Stop all activity, sit or rest?
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Tx of stable angina
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Assess the pt while performing other necessary interventions, VS, observation of respiratory distress, pain assessment, ECG?
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Tx of angina
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Administer oxygen, medication usually NTG?
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Tx of angina
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Will need lifestyle modifications and further testing if indicated?
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Tx of angina
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Cholesterol lowering, aspirin, beta-blockers, NTG, calcium channel blockers, ACE's and ARB's?
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Mediations used to treat angina
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Increase polyunsaturated fat, avoid or limit animal fat, fat should be less than 30% of diet and a doctor approved exercise regimen?
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Diet and exercise tx of angina
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Exercise, EKG, client exercises and is monitored for EKG changes?
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Stress test
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Uses dobutamine or adenosine to stimulate, exercise and monitor the EKG, must be NPO for 3 hours?
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Pharmacological stress test
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Need to be NPO, no smoking, thalium without exercise, give isotope, cold areas, ischemic or necrotic, at the end of the stress test shows ischemic areas rescan later to determine if reversible?
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Myocardial nuclear test
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Catheter is inserted into the femoral artery to look at the left side of the heart including the coronaries and into the right femoral vein to look at the right side?
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Cardiac cath
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Many potential complications, similar post care to an angiogram, check kidneys and clotting status prior?
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Cardiac cath
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This is the most serious acute coronary syndrome?
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MI
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Occurs when myocardial tissue is abruptly and severely deprived of oxygen, can effect one or all three layers of the heart?
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MI
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Dynamic process that does not occur instantly but evolves over several hours, may depend on colateral circulation and the workload of the heart?
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MI
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Obstruction of blood flow to the myocardium, plaque occludes lumen, ruptures and forms emboli, zone of necrosis, zone of injury, zone of ischemia?
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Progression of mi
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Crushing oppressive or constricting feeling, pressure that may radiate to left arm, neck, and jaw, intrascapular or epigastric pain?
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Signs and symptoms of acute MI
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Nausea, vomiting, diaphoresis, palpitations, dyspnea, cool clammy skin with low grade fever, anxiety, fear?
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Signs and symptoms AMI
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Diabetic pts may not have classic symptoms, may have dyspnea or palpitations?
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Signs and symptoms AMI
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Fatigue, back pain, nausea, vomiting, dyspnea?
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AMI symptoms in women
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Elderly may have confusion and fever?
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Elderly AMI symptoms
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Many may go into denial and not seek help for several hours?
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AMI
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12 lead ECG should be taken and reviewed by an experienced physician within ten minutes of a pts arrival in the emergency dept.?
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AMI dx
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Necrotic zone, Q or QS wave, injury zone, segment ST elevation, ischemic zone ST segment depression, inverted T wave, if no changes repeat at intervals?
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EKG AMI
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Tropin INT, creatinine kinase or CKMB, myoglobin?
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Serum cardiac markers that are most accurate in MI
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A muscle protein, the most accurate marker of MI, appears in the blood stream 4 to 12 hours after onset or injury, peaks at 12 hrs and remains elevated for 4 to 10 days?
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Tropinin I&T serum cardiac marker
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This one is an isoenzyme released after tissue necrosis, rises with 4 to 6 hours, peaks at 12 to 24 hours, returns to normal within 72 to 96 hours, is sensitive but not specific?
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Creatin Kinease CKMB cardiac marker
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Cardiac skeleltal muscle protein, not cardiac specific, but aids in dx of AMI, elevates within 2 to 4 hours, returns to normal within 24hrs?
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Myoglobin serum cardiac marker
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If initial tests for serum markers are negative, repeat in ?
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6 to 8 hour intervals depending on the symptoms
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Portable chest x-ray, trans-thoracic or tran-esophageal echocardiograph and CT?
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Other dx tools recommended in MI
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Time is muscle
12 lead EKG Draw labs Vitals and O2 Give oxygen Give aspirin Treat pain with nitro or morphine Goal is zero pain ? |
Nursing responsibilities AMI
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This is the leading cause of death in most clients with AMI who die before they can be hospitalized?
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Dysrythmias
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Identify dysrythmias, assess hemodynamic status, evaluate for discomfort?
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Interventions to potential death due to dysrythmia and MI
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Initial dose of 160 to 325mg, give ASAP unless contraindicated, should be non enteric coated, inhibits platelet activity at site of plaque rupture?
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Seven components of care #1, early aspirin
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Maintenance of 74 to 162mg a day, reduces risk of re-infarction?
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7 components of care #2, aspirin at discharge
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Receiving within 24hrs of AMI, reduces mortality in the first week by 14%, contraindicated if heart rate is less than 50, pr interval greater than 0.24?
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7 components of care #3 MI, early beta-blocker therapy
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Reduces long term mortality by 23%, drug selection is based on the desired mechanism of action?
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7 components of care #4 MI, beta-blockers at discharge
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At discharge for pts with dystolic dysfunction, causes vasodilation reducing afterload, contraindicated in renal artery stenosis?
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7 components of care #5 MI, ACE or ARB's at discharge for pts with dystolic dysfunction
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Fibrinolysis with tissue plaminogen (activase) activator to lyse thombus
- to be a candidate, pt must have STEMI and symptoms within 12hrs - door-to-needle time is 30 min. or less Percutaneous coronary interventions - consists of coronary arteriography and percutaneous coronary balloon angioplasty - should be performed within 90 min. of pts arrival PTCA preferable if available??? |
7 components of care #6 MI, Timely reperfusion stratagies
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The five A's
Ask every pt about tobacco use Advise every pt to quit Assess if they are willing to try and quit within the next 30 days Assist with quitting plan Arrange follow up within 1 week of quitting? |
7 components of care #7 MI, counseling to stop smoking
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Restoration of perfusion to the injured area often limits the amount of extension and improves left ventricle function?
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Reasons for timely reperfusion stategies in MI
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Complete sustained reperfusion of coronary arteries within the first few hours after MI?
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This will decrease the mortality rate
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denigrate
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blacken; *to belittle*
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Fiberin specific and 3 to 5 minutes half-life, indications are within six hours of pain, containdications are bleeding, recent surgery, recent CVA, GI bleeding, watch for bleeding, give platelet inhibitors?
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Fibrolinc therapy
Activase Retroplase Tenecteplase |
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Abrupt cessation of pain, sudden onset of ventricular dysrythmia, just monitor, 12 hour peak of cardiac markers, may need heparin to prevent reocclusion, go home on antiplatelets?
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Identification of coronary artery reprofusion
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This prevents fibrogen from attaching to the activated platelets at the thrombus, used alone or with fibrinolytics and/or PTCA?
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Glycoprotein inhibitors
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Compresses atheroma and stretches coronary artery?
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PTCA
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Inserted after a PTCA to keep vessels open?
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Coronary artery stent
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Removal of plaque with a laser or rotary cutting head?
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Atherectomy
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Monitor for pain, may reocclude, if so, call the doctor and treat as an MI?
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Caution in invasive coronary artery procedures
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This utilizes another vein to bypass a diseased coronary artery?
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Coronary artery revascularization
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Can be done on or off bypass pump, no opinions on which is better?
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Coronary artery revascularization
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Watch for decreased cardiac output, Afib, ventricular arrythmias, heart block, pericardial effusion and tamponade?
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Caution with coronary artery bypass graft or CRBG
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RESP-Atilectasis, pleural effusion overload (VAP), pain control opiods and NSAIDS, coagulation bleeding post-op, risk for DVT or PE?
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Cautions with coronary artery bypass graft
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Renal needs to maintain perfusion and avoid fluid overload, could cause peptic ulcer, pancreatitis, mesenteric ischemia, follow best wound care practices?
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Cautions with coronary artery bypass graft
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Assess pts anxiety but encourage expression of anxiety, try to define origin of anxiety, give simple explanations of therapy, help with coping enhancement?
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Ineffective coping enhancements (CABG)
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Cardiac rehab, exercise, reduction risk factors?
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Activity intolerance intervention, CABG
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Assess, monitor VS and perfusion, monitor hemodynamics, complications and educate the pt on signs and symptoms to watch for?
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Potential for heart failure interventions
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Obtain tests, give oxygen, aspirin, nitroglycerin, morphine, beta-blockers, ACE within 24hrs, evaluate for percutaneous coronary intervention or fibrinolynic therapy, if indicated IV heparin or lmwh, Clopidogrel or Ticlopidine, glycoprotein inhibitor, bedrest?
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MI treatment
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Stop smoking, control diet, complimentary and alternative therapies, physical and sexual activity?
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Discharge teaching MI
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Blood pressure control, blood glucose control, take your medications, self monitor, seek medical help when needed?
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Discharge teacing MI
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The ability of the cell to spontaneously and repeatedly generate and discharge an electrical charge. This is where the electricity starts?
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Automaticity
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The ability of the cell to respond to the electrical stimulation and to depolarize?
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Excitability
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The ability of the cell to shorten and lengthen the muscle? The mechanical part.
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Contractibility
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Depolarization and repolarization? In other words its sending out the charge and resetting for the charge.
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Action Potential
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The ability to transfer the pulse from cell to cell?
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Conductivity
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Sodium flows into the cell and is followed by calcium and then magnesium during?
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Depolarization
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What is the gate keeper that controls the amount of sodium flowing into the cell?
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Calcium
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When does potassium shift out of the cell?
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During repolarization?
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What follows potassium out of the cell during repolarization?
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Sodium
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SA node to AV node, left and right bundle of His, Purkinge fibers?
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The electrical pathway
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Where is the SA node located?
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In the rear portion of the right atrium
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What is located between the atrium and the ventricles?
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The AV node
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Look at the patient!
EKG Lab Work History Medications Diagnostic Exams |
Assessment of a chest pain patient
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The amount of blood that is squeezed out from the left ventricle when it contracts?
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Ejection Fraction (EF)
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What represents the atrial depolarization?
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P wave
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What represents a depolarization and impulse travel through the conduction system?
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PR Interval
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What represents ventricular depolarization?
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QRS complex
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These represent the states of ventricular repolarization?
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ST segment, T wave and Uwave
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This interval represents the total time of depolarization and repolarization?
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QT interval
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0.12 - 0.20?
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Normal PR interval (PRI)
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0.06 - 0.10?
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Normal QRS complex duration
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0.36 - 0.44?
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Normal QT interval
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1 small square on EKG stands for?
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0.04 seconds
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1 large square on EKG stands for?
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0.20 seconds
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5 large boxes on an EKG equals?
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1 second
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Atrial rhythm: grossly irregular
Vent. rhythm: grossly irregular Atrial rate: greater than 400 bpm Vent. rate: 60-150 bpm depending on treatment P wave: absent; appearance of erratic baseline fibrillatory waves PR interval: indiscernible T wave: indiscernible QT interval: not measurable ? |
Atrial fibrillation
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If the pt is symptomatic,synchronized cardioversion should be used immediately, then anticoagulation therapy and possibly oxygen, cardizem, amiodarone, calcium channel blockers?
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Atrial fibrillation intervention
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|
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Ventricular rhythm may be regular or irregular
Atrial rate: 300 to 350 bpm Ventricular rate: variable P wave: atrial activity seen as flutter waves, often with a saw-toothed appearance PR interval: not measurable QRS complex: can be distorted by the underlying waves T wave: unidentifiable QT interval: not measurable |
Atrial flutter
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|
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Calcium channel blockers
Beta-blockers Digoxin |
Atrial flutter intervention
|
|
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May interact with beta blockers or calcium channel blockers resulting in an excessively slow heart rate, or a block in conduction of the electrical impulse through the heart?
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Amiodarone
|
|
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Increases the blood level of digoxin when the two drugs are given together. It is recommended that digoxin dosage be cut by 50% when this therapy is started?
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Amiodarone
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This drug can result in dilantin toxicity because it causes 2-3 fold increase in blood concentration of dilantrin?
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Amiodarone
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The drug can interact with tricyclic antidepressants and potentially cause life threatening arrhythmias?
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Amiodarone
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This drug interacts with coumadin to increase the risk of bleeding. This effect can occur as early as 4-6 days after starting the combination of drugs?
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Amiodarone
|
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Because it stays in the body for a long time, drug interactions are possible weeks after the discontinuation of the drug?
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Amiodarone
|
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Long term use of this drug can cause lung and liver toxicity. Chest x-ray and liver function tests are recommended every 4-6 months?
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Amiodarone
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8 out of 10 pts taking this drug will experience a side effect?
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Amiodarone
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Provides
|
pacemaker
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Components:
a. pulse generator with circuitry - power source b. the lead-delivers the electrical impulse generator to the myocardium c. electrode system ? |
pacemaker
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|
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The heart is stimulated through large gelled electrode pads placed anteriorly and posteriorly?
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External (transcutaneous) pacing
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The electrical energy travels from an external impulse generator through the throacic musculature directly to the epicardial surface of the heart of the heart via lead wires?
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Epicardial (transthoracic) pacing
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Lead dislodgment, microshock, cardiac Tamponade, infection, psychological reactions, failure to sense, failure to capture?
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Complications with epicardial (transthoracic) pacing
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|
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The surgeion inserts the pacing electrode via the transvenous route, and threads the electrode into the right atrium or right ventricle so that it comes into direct contact with the endocardium?
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Endocardial (trasvenous) pacing
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Thrombophlebitis, infection, sepsis, lead displacement, discomfort of having an extremity near insertion site immobilized, perforation, failure to sense, failure to capture, myocardial irritability, hiccups, abdominal twitching?
|
Complications of endocardial (transvenous) pacing
|
|
|
May be used in emergency or elective situations that require limited, short term pacing. An external generator is used for this, and leads can be applied through any of the above methods?
|
Temporary pacing
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|
|
Treatment focuses on finding the primary cause. If it's high catecholamine levels, a beta-adrenergic blocker may slow the heart rate. After myocardial infarction, it may precede heart failure or cardiogenic shock.
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Sinus tachycardia
|
|
|
Atrial rhythm: regular
Ventricular rhythm: regular Atrial rate: 100 to 160 bpm P wave: As the rate reaches about 150 bpm, the P wave merges with the preceding T wave and may be difficult to identify. Examine the descending slope of the preceding T wave closely for notches, indicating the presence of the P wave. Other: gradual onset and cessation |
Sinus tachycardia
|
|
|
If the pt is asymptomatic, treatment isn't necessary. If he has signs and symptoms, treatment aims to identify and correct the underlying cause. The heart rate may be increased with such drugs as atropine and isoproterenol (Isuprel). A temporary or permanent pacemaker may be inserted if the bradycardia persists.
? |
Sinus bradycardia
|
|
|
Atrial rate: less than 60 bpm
Vent. rate: less than 60 bpm |
Sinus bradycardia
|
|
|
This rhythm often degenerates into ventricular fibrillation and cardiovascular collapse, requiring immediate cardiopulmonary resuscitation and defibrillation. If the pt is symptomatic, prepare for immediate cardioversion, followed by antiarrhythmic therapy. Lidocaine (Xylocaine) is usually administered immediately. If it proves ineffective, procainamide (Pronestyl) or bretylium (Bretylol) is used?
|
Ventricular tachycardia
|
|
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Atrial rhythm: p waves probably not visible or independent P waves possibly discernible with slower ventricular rates
Ventricular rhythm: usually regular but may be slightly irregular Atrial rate: can't be determined Ventricular rate: usually 100 to 200 bpm P wave: usually absent; possibly obscured by the QRS complex; retrograde P waves possible presence PR interval: not measurable QRS complex: duration greater than 0.12 second; bizarre appearance, usually with increased amplitude T wave: opposite the terminal forces of the QRS complex QT interval: not measurable |
Ventricular tachycardia
|
|
|
Perform cardiopulmonary resuscitation until the pt can receive defibrillation. Administer epinephrine if initial defibrillation series is unsuccessful. Other drugs that may be used include lidocaine (Xylocaine), bretylium (Bretylol), and procainamide (Pronestyl). Magnesium sulfate may be used for torsades de pointes or refractory ventricular fibrillation?
|
Ventricular fibrillation
|
|
|
Atrial rhythm: can't be determined
Ventricular rhythm: irregular Atrial rate: can't be determined Ventricular rate: can't be determined P wave: indiscernible PR interval: not measurable QRS complex: replaced with fibrillatory waves; duration not discernable T wave: can't be determined QT interval: not measurable |
Ventricular fibrillation
|
|
|
Treatment aims to identify and manage the primary problem that triggered this safety mechanism. Atropine or dopamine (Intropin) may be given to increase the atrial rate. A pacemaker may also be inserted to increase the heart rate and thereby improve cardiac output?
|
Idioventricular rhythm
|
|
|
Atrial rhythm: can't be determined
Ventricular rhythm: usually regular, except with isolated escape beats Atrial rate: unable to be determined Ventricular rate: less than 40bpm P wave: absent PR interval: usually not measurable QRS complex: duration greater than 0.12 second; complex is wide and has a bizarre configuration T wave: directed opposite terminal forces of QRS complex QT interval usually greater than 0.44 second |
Idioventricular rhythm
|
|
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PR interval: greater than 0.20 second and constant
|
First degree AV block
|
|
|
If the pt is asymptomatic; no intervention is required other than monitoring the electrocardiogram frequently to see if a more serious form develops. If the pt is symptomatic; the doctor may order atropine to increase the rate and to stop the decremental conduction through the AV node. Occasionally, the doctor may insert a temporary pacemaker to maintain an effective cardiac output.
|
Second-degree atrioventricular block, type 1
|
|
|
Ventricular rhythm: irregular
Atrial rate: determined by the underlying rhythm Ventricular rate: slower than the atrial rate PR interval: progressively prolonged with each beat until a P wave appears without a QRS complex QRS complex: periodically absent Other: usually distiguished by a pattern of group beating, referred to as the footprints of Wenckebach? |
Second-degree atrioventricular block, type 1
|
|
|
If the pt is hypotensive, treatment aims at increasing his heart rate to improve cardiac output. Because the conduction block occurs in the His-Purkinje system, drugs that act directly on the myocardium usually prove more effective than those that increase the atrial rate. As a result, dopamine (Intropin) instead of atropine may be ordered to increase the ventricular rate.
If the pt has an anterior wall MI, the doctor will immediately insert a temporary pacemaker to prevent ventricular asystole. For long-term managment, the pt usually needs a permanent pacemaker. |
Second-degree atrioventricular block, type 2
|
|
|
Ventricular rhythm: regular or irregular
Ventricular rate: may be within normal limits but less than the atrial rate QRS complex: usually greater than 0.16 second because of the presence of a preexisting bundle-brance heart block |
Second-degree atrioventricular block, type 2
|
|
|
If cardiac output isn't adequate or the pt's condition is deteriorating, the doctor will order therapy to improve the ventricular rhythm. Initially, atropine may be ordered to increase the ventricular rate and improve cardiac output until a pacemaker is available?
|
3rd degree AV block
|
|
|
Atrial rhythm: usually regular
Ventricular rhythm: usually regular Atrial rate: usually within normal limits Ventricular rate: slow PR interval: not measurable because the atria and ventricles beat independently of each other QRS complex: determined by the site of the escape rhythm (With a junctional escape rhythm, the duration and configuration are normal; with an idioventricular escape rhythm, the duration is greater than 0.12 second and the complex is distorted) QT interval: may or may not be within normal limits |
3rd degree AV block
|
|
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Decreased the clotting ability of the blood. Sometimes called blood thinners, although they do not actually thin the blood. They do NOT dissolve existing blood clots. Used to treat certain blood vessel, heart and lung conditions?
|
Anticoagulants (Blood Thinners)
|
|
|
Dalteparin (Fagmin)
Danaparoid (Orgaran) Enoxaparin (Lovenox) Heparin (various) Tinzaparin (Innohep) Warfarin (Coumadin) ? |
Anticoagulants (Blood Thinners)
|
|
|
Helps to prevent harmful clots from forming in the blood vessels. May prevent the clots from becoming larger and causing more serious problems. Often prescribed to prevent first or recurrent stroke?
|
Anticoagulants (Blood Thinners)
|
|
|
Commonly prescribed include:
Aspirin, Ticlopidine, Clopidogrel and Dipyridamole? |
Antiplatelet Agents
|
|
|
Keeps blood clots from forming by preventing blood platelets from sticking together?
|
Antiplatelet Agents
|
|
|
Helps prevent clotting in pts who have had a heart attack, unstable angina, ischemic strokes, TIA and other forms of cardiovascular disease. Usually prescribed preventively, when plaque buildup is evident but there is not yet a large obstruction in the artery?
|
Antiplatelet Agents
|
|
|
Commonly prescribed include:
Benazepril (Lotensin) Captopril (Capoten) Enalapril (Vasotec) Fasinopril (Monopril) Lisinopril (Prinivil, Zestril) Moexipril (Univasc) Perindorpril (Aceon) Quinapril (Accupril) Ramipril (Altace) Trandolapril (Mavik) ? |
Angiotensin-Converting Enzyme (ACE) Inhibitors
|
|
|
Expands blood vessels and decreases resistance by lowering levels of angiotensin II. Allows blood to flow more easily and makes the heart's work easier or more efficient?
|
Angiotensin-Converting Enzyme (ACE) Inhibitors
|
|
|
Used to treat or improve symptoms of cardiovascular conditions including high blood pressure and heart failure?
|
Angiotensin-Converting Enzyme (ACE) Inhibitors
|
|
|
Commonly prescribed include:
Candesartan (Atacand) Eprosartan (Teveten) Irbesartan (Avapro) Losartan (Cozaar) Telmisartan (Micardis) Valsartan (Diovan) ? |
Angiotensin II Receptor Blockers (or Inhibitors) (Also known as ARBs, Angiotensin-2 Receptor Antagonists and AT-2)
|
|
|
Rather than lowering levels of angiotensin II (as ACE inhibitors do) angiotensin II receptor blockers prevent this chemical from having any effects on the heart and blood vessels. This keeps blood pressure from rising?
|
Angiotensin II Receptor Blockers (or Inhibitors) (Also known as ARBs, Angiotensin-2 Receptor Antagonists and AT-2)
|
|
|
Used to treat or improve symptoms of cardiovascular conditions including high blood pressure and heart failure?
|
Angiotensin II Receptor Blockers (or Inhibitors) (Also known as ARBs, Angiotensin-2 Receptor Antagonists and AT-2)
|
|
|
Commonly prescribed include:
Acebutolol (Sectral) Atenolol (Tenormin) Betaxolol (Kerlone) Bisoprolol/hydrochlorothiazide (Ziac) Bisoprolol (Zebeta) Carteolol (Cartrol) Metoprolol (Lopressor, Toprol XL) Nadolol (Corgard) Propranolol (Inderal) Sotalol (Betapace) Timolol (Blocadren) ? |
Beta Blockers
|
|
|
Decreases the heart rate and cardiac output, which lowers blood pressure and makes the heart beat more slowly and with less force?
|
Beta Blockers
|
|
|
Used to lower blood pressure. Used with therapy for cardiac arrhythmias (abnormal heart rhythms) and in treating chest pain (angina).
Used to prevent future heart attacks in pts who have had a heart attack? |
Beta Blockers
|
|
|
Commonly prescribed include:
Amlodipine (Norvasc, Lotrel) Bepridil (Vascor) Diltiazem (Cardizem, Tiazac) Felodipine (Plendil) Nifedipine (Adalat, Procardia) Nimodipine (Nimotop) Nisoldipine (Sular) Verapamil (Calan, Isoptin, Verelan) ? |
Calcium Channel Blockers
|
|
|
Interrupts the movement of calcium into heart and vessel cells. May decrease the heart's pumping strength and relax blood vessels?
|
Calcium Channel Blockers
|
|
|
Used to treat high blood pressure, chest pain (angina) caused by reduced blood supply to the heart muscle and some arrhythmias (abnormal heart rhythms).
|
Calcium Channel Blockers
|
|
|
Commonly prescribed include:
Amiloride (Midamor) Bumetanide (Bumex) Chlorothiazide (Diuril) Chlorthalidone (Hygroton) Furosemide (Lasix) Hydrochlorothiazide (Esidrix, Hydrodiuril) Indapamide (Lozol) Spironolactone (Aldactone) ? |
Diuretics (Also known as Water Pills)
|
|
|
Caused the body to rid itself of excess fluids and sodium through urination. Helps to relieve the heart's workload. Also decreased the buildup of fluid in the lungs and other parts of the body, such as the ankles and legs. Different diuretics remove fluid at varied rates and through different methods?
|
Diuretics (Also known as Water Pills)
|
|
|
Used to help lower blood pressure. Used to help reduce swelling (edema) from excess buildup of fluid in the body?
|
Diuretics (Also known as Water Pills)
|
|
|
Isosorbide dinitrate (Isordil)
Nesiritide (Natrecor) Hydralazine (Apresoline) Nitrates Minoxidil ? |
Vasodilators (Also known as Nitrates. Nitroglycerin tablets are a form of vasodilator.)
|
|
|
Relaxes blood vessels and increases the supply of blood and oxygen to the heart while reducing its workload. Prescribed to pts who cannot tolerate ACE inhibitors (another type of medicine that relaxes the blood vessels.)
Can come in pills to be swallowed, chewable tablets and a a topical application (cream). |
Vasodilators (Also known as Nitrates. Nitroglycerin tablets are a form of vasodilator.)
|
|
|
Used to ease chest pain (angina).
|
Vasodilators (Also known as Nitrates. Nitroglycerin tablets are a form of vasodilator.)
|
|
|
Commonly prescribed include:
Lanoxin |
Digitalis Preparations (Also known as Digoxin and Digitoxin)
|
|
|
Increases the force of the heart's contractions, which can be beneficial in heart failure?
|
Digitalis Preparations (Also known as Digoxin and Digitoxin)
|
|
|
Used to relieve heart failure symptoms, especially when the pt isn't responding to ACE inhibitors and diuretics. Also slows certain types of irregular heartbeat (arrhythmias), particularly atrial fibrillation?
|
Digitalis Preparations (Also known as Digoxin and Digitoxin)
|
|
|
Various medications can lower blood cholesterol levels. They may be prescribed individually or in combination with other drugs. They work in the body in different ways. Some affect the liver, some work in the intestines and some interrupt the formation of cholesterol from circulating in the blood?
|
Statins - Common types of cholesterol-lowering drugs include statins, resins and nicotinic acid (niacin), gemfibrozil and clofibrate.
|
|
|
Used to lower LDL ('bad") cholesterol, raise HDL ("good") cholesterol and lower triglyceride levels?
|
Statins - Common types of cholesterol-lowering drugs include statins, resins and nicotinic acid (niacin), gemfibrozil and clofibrate.
|
|
|
Atrial flutter has how many origins?
|
1
|
|
|
Atrial flutter rate range?
|
240-360 bpm
|
|
|
The AV Node is completely blocking of communication between the atrium and the ventricle?
|
Complete Heart Block (3rd degree heart block)
|
|
|
Where the atrium has a pulse and the ventricle has a pulse but they are independent of each other (no connection)?
|
Complete Heart Block (3rd degree heart block)
|
|
|
This drug suppresses the ventricular irritability?
|
Lidocaine
|
|
|
Is Lidocaine given in complete heart block (3rd degree heart block)?
|
NEVER!
|
|
|
No P wave and it will be slow?
|
Injunctional rhythm (where the SA node drops the ball and the AV node makes up for it)
|
|
|
What side of the chest does a pacemaker usually go on?
|
The non-dominant side (usually left)
|
|
|
Pt teaching; procedure and purpose of
assess vital signs and heart rhythm secure and check all connections monitor battery and control settings clean and dress the incision site keep generator dry and secure to pt protect pt from microshock, maintain grounding limit motion of extremity at insertion site monitor pacemaker function, settings document ? |
Nursing care for pacemaker pts
|
|
|
Indicated for chronic or recurrent Dysrhythmias that are severe or unresponsive to medication?
|
Permanent Pacing
|
|
|
Pacemaker modes:
designed to fire constantly at a preset without regard to the pt's own electrical activity? |
Fixed
|
|
|
Pacemaker modes:
having a sensing device that senses the heart's electrical activity and fires at a preset rate only when the heart's rate drops below a predetermined level? |
Demand
|
|
|
A pacing spike is seen. With atrial pacing, a P wave follows the spike, but may be hidden in some leads. The ECG with ventricular pacing shows an abnormal QRS complex because the impulse begins in the ventricle?
|
Electrocardiography of paced beats
|
|
|
Special telephone equipment is able to monitor the pt's ECG. The transmitter converts the pt's elecrical activity and pacemaker artifacts to audio tones for transmission via telephone to an ECG receiver. The reciver provides an ECG strip recording and pritout of the electrical activity of the pt's implanted pacemaker?
|
Transtelephonic pacemaker
|
|
|
Pacemaker failure:
The inability of the sensor to detect the pt's intrinsic beats and thus the pacemaker sends out impulses too early? |
Pacemaker failure: failure to sense
|
|
|
Pacemaker failure:
A disorder in the pacemaker electrodes; the impulse does not generate depolarization? |
Pacemaker failure: failure to capture
|
|
|
Pacemaker failure:
Malfunction of the pulse generator. The ECG shows a lack of any impulse? |
Pacemaker failure: failure to pace
|
|
|
What are the clinical manifestations of pacemaker malfunction?
|
Syncope, bradycardia or tachycardia, and palpitations.
|
|
|
6 sinus syndrome, where does it occur?
|
In the SA node.
|
|
|
What does a person that has 6 sinus syndrome get?
|
A pacemaker
|
|
|
What does a flattened P wave with a high, peaked T wave indicate?
|
Hyperkalemia
|
|
|
When handling pacemaker wires what should you wear?
|
Gloves
|
|
|
If you have a pt with a lot of PVC just out of nowhere, what should you do?
|
Run an electrolyte test to see if they have elevated potassium levels?
|
|
|
One to One care?
|
1 nurse, 1 pt
|
|
|
Vital signs every 15 minutes to one hour?
|
Open Heart Post-op
|
|
|
Most common frequent labs for Post-op Heart Surgery Pt's?
|
Lytes, Hemoglobin, and HNH
|
|
|
A line placed in the radial, femoral or brachial artery to monitor blood pressure?
|
Intraaortic Blood Pressure
|
|
|
The biggest risks with intraaortic blood pressure line?
|
Bleeding, infection, damage to the arterial wall, and altered tissue perfusion
|
|
|
Intra-arterial pressures and cuff pressures should not be more than what apart?
|
10 mmHG
|
|
|
Putting a catheter into the heart through the subclavian or jugular vein allows us to monitor heart function, take measurements and get accurate pressures of the heart?
|
Pulmonary artery catheter (SWANS)
|
|
|
Pulmonary artery catheter measurement of the right atrium is?
|
Pulmonary Artery Catheter
CVP - right atrium |
|
|
A low CVP or preload?
|
Indicates low fluid volume in the body.
|
|
|
A high CVP or preload?
|
Indicates fluid overload
|
|
|
A catheter that assists the ventricle to work properly?
|
A ventricular assist device or VAD
|
|
|
A bridge to transplant?
|
Ventricular assist device or VAD
|
|
|
Used to per-fuse coronary arteries?
|
Intraaortic Balloon Pump
|
|
|
Balloon inflates with every heartbeat to per-fuse coronary arteries?
|
Intraaortic Balloon Pump
|
|
|
Get them off within 4 hours or at least by the next morning?
|
Ventilation
|
|
|
Chest tube output should be monitored?
|
hourly
|
|
|
Besides vital signs and pulses, what other assessment is important for post heart surgery.
|
I&O
|
|
|
#1 bug that causes rheumatic fever?
|
Strep
|
|
|
All layers of the heart are affected by this inflammatory disease?
|
Rheumatic Fever
|
|
|
What is the first thing we do when a pt comes in?
|
History and EKG
|
|
|
EKG/Echo
MRI Chest Xray Heart Cath Stress Test Nuclear studies Calcium Score ? |
Diagnostics for heart disease
|
|
|
Gold standard in heart care diagnostics?
|
Cardiac Cath
|
|
|
Whenever you hear a murmur, your first thought should be?
|
Valves
|
|
|
Virus most commonly involved in Pericarditis?
|
Cocksackie Virus B
|
|
|
The pericardial space holds how much fluid?
|
20-50cc
|
|
|
Cocksackie virus B
Post MI Renal Disease Autoimmune Drug reactions ? |
Pericarditis
|
|
|
Fever / chest pain
Friction rub Pleural effusion on CXR? |
Symptoms of Pericarditis
|
|
|
Fluid in the pericardial sac?
|
Pleural Effusion
|
|
|
JVD
Decreasing Blood Pressure Muffled heart tones |
Becks Triad
|
|
|
Rapid collection of fluid in the pericardial sac?
|
Cardiac Tamponade (very dangerous)
|
|
|
Emergency removal of fluid from the pericardial sac due to tamponade?
|
Pericardiocentesis
|
|
|
Irritated ventricles will cause?
|
V tach
|
|
|
An intentional hole placed in the pericardium to relieve rapid filling fluid?
|
Pericardial Window
|
|
|
Cardiac tamponade is a complication of what?
|
Pericardial effusion
|
|
|
Hemodynamic monitoring
Assessment Monitor EKG REPORT CHANGES manage anxiety ? |
Nursing managements of pericardial effusion
|
|
|
Inflammation of the myocardium?
|
Myocarditis
|
|
|
Radiation and chemotherapy sometimes can cause?
|
Myocarditis
|
|
|
Most popular cause of myocarditis is?
|
Cocksackie Virus B
|
|
|
Severe cases of myocarditis may lead to?
|
Cardiomyopathy
|
|
|
Fatigue
Shortness of breath Fever Aching joints Palpitations Rhythm issues |
Heart disease symptoms
|
|
|
May use any of the heart meds plus these two in myocarditis?
|
Antibiotics and Steroids
|
|
|
These are controversial and can cause myocardial damage in some cases?
|
NSAIDS
|
|
|
There is valve involvement?
|
Infective Endocarditis
|
|
|
Infection embeds itself in the matrix of the valves causing malfunction, vegetation (will require TEE)?
|
Infective Endocarditis
|
|
|
Will find vegetation in valve damage?
|
TEE
|
|
|
Staff, strep, graham negative bacterias are common causes of?
|
Infective Endocarditis
|
|
|
Fever, headache, GI, weight loss, fatigue, arrhythmias, general aching, murmur, skin problems?
|
Infective Endocarditis
|
|
|
Heart infections cause disruption of the flow of blood from the heart which is why we use what type of drugs?
|
Anticoagulants
|
|
|
Frequent rest periods, infection prevention, space activity, VS, peripheral pulses, EKG, skin, cap refill, i&o?
|
Nursing intervention
|
|
|
Fatigue, diminished activity, decreased cardiac output?
|
Nursing dx
|
|
|
Usually caused by inflammation, opening of the valve will narrow?
|
Stenosis
|
|
|
Leaflets are unable to close causing blood?
|
Regurgitation
|
|
|
One leaflet that is dysfunctional causing regurgitation is?
|
Prolapse
|
|
|
Most common prolapse?
|
Mitral valve
|
|
|
Left atrium dilitation, pulmonary congestion, right sided heart failure?
(Chronic) |
Stenotic Mitral valve
|
|
|
All valve problems lead to?
|
Heart failure
|
|
|
Can be acute or chronic, mostly chronic, left atrium dlitation, pulmonary congestion, right sided heart failure (valve won't close)?
|
Mitral Regurgitation
|
|
|
Dilitation of the left ventricle, hypertrophy of the left ventricle, Left heart failure first then right?
|
Aortic Stenosis
|
|
|
Can be asymptomatic for 20 years, gradual hypertrophy, left atrium dilitation, pulmonary congestion, right sided heart failure?
|
Aortic Regurgitation
|
|
|
Very rare, leads to right sided heart failure?
|
Tricuspid Stenosis
|
|
|
Backs up into the right atrium, caused by pulmonary HTN, both chambers will be involved but you will have right sided heart failure?
|
Tricuspid Regurgitation
|
|
|
Narrowing of valve, right sided heart failure?
|
Pulmonary Stenosis
|
|
|
Most common cause is endocarditis,
|
Pulmonary Regurgitation
|
|
|
The repair of the rings at the junction of the valve, for regurgitation?
|
Annuloplasty
|
|
|
Repairs the leaflets in the supporting tissue of the valve, stenosis?
|
Valvuloplasty
|
|
|
A catheter and balloon way of doing annuloplasty and valvuloplasty?
|
PTBV
|
|
|
Replacement is if you are pregnant or old, unable to take anticoagulants?
|
Prosthetic heart valve replacement tissue
|
|
|
If the EF is below 35%, you become?
|
A transplant candidate
|
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If you are a younger person with valve problems, not having a problem taking anticoagulants, not interested in getting pregnant, will take anticoagulants for the rest of life?
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Prosthetic heart valve replacement mechanical
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When annuloplasty and valvuloplasty do not work?
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Prosthetic heart valve replacement
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Tissue valves come in?
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Pork, Beef and Human
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Tissue valve recipients need to be on what medication?
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Immunosuppresants because their body might try to reject it. They will be on anticoagulants initially but not forever.
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A disease of the myocardial muscle fibers, causes functional and structural damage, is progressive, causes are recreational drugs, alcohol, chemotherapy, HTN, post partum, congenital?
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Cardiomyopathy
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Most common type, fibrosis of the muscle that leads to poor contractility, chambers over fill, hypertrophy (thicken), reduces stroke volume which reduces cardiac output, may do a muscle biopsy, may have bundle branch block?
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Cardiomyopathy
dilated |
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Disorder of the sarcomere, sarcomere contractile part of the muscle, ventricle hypertrophy, large septum, low end diastolic volume, can lead to aortic obstruction, usually genetic, most common in young adults, chest pain, syncope?
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Cardiomyopathy
Hypertrophic Obstuctive |
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Least common, results from scarring of the endocardium, could have been caused by endocarditis, radiation or drug use, restricts one or both of the ventricle walls, they become thickened, filling pressures increase, dilitation in the atrium, may get a pacer?
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Cardiomyopathy
Restrictive |
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Bundle branch block?
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Widened QRS
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Powerlessness and altered coping?
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Nusing Dx for Cardiomyopathy
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For many myocardial pts, the only treatment is?
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Transplangt
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Shortage, tissue rejection, size, antibodies, only 6 hours to get done?
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Problems with Transplant
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Must be on immunosuppresant therapy for the rest of their lives, steroids, cyclosporins, infection an malignancy are risks for immunosuppresants?
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Transplant recipients
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Immediate, acute and chronic?
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Transplant rejection
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Immediate transplant rejection is?
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fatal
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Acute transplant rejection can be?
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treated with meds
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Chronic transplant rejection will require?
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Medications and frequent monitoring (every 6 months, myocardial biopsy)
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