Basic ECG Module

Cardiac DisordersChabot Nursing ProgramNursing 60 BSpring 2015Nursing 60BSpring 2014Cardiovascular ObjectivesDiscuss tests/studies used in the assessment of the cardiovascular system, to include the following: a. Laboratory tests b. Cardiac Catheterization c. Echocardiography d. Myocardial Nuclear Perfusion Imaging e. Exercise Electrocardiography (Stress test) f. Hemodynamic monitoring2. Review presentation/treatment of lethal dysrhythmias3. Discuss critical nursing assessments and interventions in the care of the client who has undergone cardiac surgery: 4. Review critical assessments and treatments in the care of the client who has pulmonary edema and congestive heart failure5. Identify common drug therapies to improve cardiac output.6. Prioritize nursing care for clients experiencing heart failure7. Compare and contrast common valvular disorders

Slide 2Cardiovascular Disorders8. Discuss surgical management for clients with valvular disease9. Develop a teaching/learning plan for clients with valvular disease10. Differentiate between common cardiac inflammations and infections-endocarditis, pericarditis, and rheumatic carditis11. Compare and contrast dilated, hypertrophic and restrictive cardiomyopathy12. Explain the pathophysiology of Acute Coronary Syndrome13. Discuss the assessment findings in clients who have ACS, and prioritize nursing care for clients who have ACS14. Discuss medications commonly used in the treatment of the client with ACS15. Prioritize nursing care for the client who has underdone CABG surgery16. Discuss the differences between CABG surgery, minimally invasive direct coronary artery bypass, and off-pump CABG.17. Identify findings in the client who has developed cardiac tamponade and critical interventions

Slide 3Slide 4Comparison of Types of Cardiomyopathies

Slide 5Cardiomyopathy Illustrations

Slide 6Dilated Cardiomyopathy Characteristics

Slide 7Dilated Cardiomyopathy Clinical Presentation

Slide 8Dilated Cardiomyopathy Management

Slide 9Dilated Cardiomyopathy

Slide 10Hypertrophic Cardiomyopathy Characteristics

Slide 11Hypertrophic Cardiomyopathy Clinical Presentation

Slide 12Hypertrophic Cardiomyopathy Management

Slide 13

Slide 14Hypertrophic Cardiomyopathy

Slide 15Restrictive Cardiomyopathy Characteristics

Causes:Buildup of abnormal proteinsin the heart muscle (amyloidosis) #1 cause in U.S.Build up of scar tissue (no known reason)Radiation or chemotherapy exposure Excess ironin the heart (hemochromatosis)Other systemic diseases (e.g.(sarcoidosis, scleroderma)Slide 16Restrictive Cardiomyopathy Clinical Presentation

Slide 17Restrictive Cardiomyopathy Management

Slide 18Heart FailureInadequacy of the heart to pump blood throughout the body; causes insufficient perfusion of body tissue with vital nutrients and oxygenLeft-sided heart failureRight-sided heart failureHigh-output failure

Congestive Heart FailureMost common cause of hospital admissions for people 65 yrs or olderMajor cause of disability and death after myocardial infarctionCommon Risk Factors:HypertensionDysrhythmiasCoronary artery disease DiabetesCardiomyopathySmokingSubstance abuseObesityValvular diseaseFamily HistoryCardiac infections, inflammation Lung DiseaseHyperthyroidism Sleep ApneaSlide 19Slide 20Left-Sided Heart FailureManifestations:WeaknessFatigueDizzinessConfusionPulmonary congestionShortness of breath(Continued)

Slide 21Right-Sided Heart FailureManifestations:Distended neck veins, increased abdominal girthHepatomegaly Hepatojugular refluxAscitesDependent edemaWeight: most reliable indicator of fluid gain or loss

Slide 22Heart Failure Assessments Laboratory assessmentElectrolytes, BUN, H & H, B-type natriuretic peptideUA for protein, microalbuminABG to assess hypoxemia Radiographic assessmentCardiomegaly, rule out respiratory causesEchocardiographyValves, ventricles, HF Ejection Fraction < 40

22B-type Natriuretic peptide (BNP) diagnostic of HF with assessment, may be elevated in patients with renal disease BNP is secreted from the ventricles of the heart in response to changes in pressure that occur when heart failure develops and worsensBNP levels below 100 pg/mL indicate no heart failure.BNP levels of 100-300 pg/mL suggest heart failure is present.BNP levels above 300 pg/mL indicate mild heart failure.BNP levels above 600 pg/mL indicate moderate heart failure.BNP levels above 900 pg/mL indicate severe heart failure.Chest X-ray for cardiomegalyEchocardiography evaluates valvular changes, pericardial effusion, chamber enlargement and ejection fracture Ejection fraction N 55-70 90%Morphine during acute phase anxietyAngiotensin-converting enzyme inhibitors enalapril (Vasotec), fosinopril (Monopril)Angiotensin Receptor Blockers valsartan (Diovan), irbesartan (Avapro) losartan (Cozaar)Diuretics furosemide, bumetanide, observe for potassium deficiency and give replacements; for mild fluid overload hydrocholorothiazide, metolzazon (Zaroxolyn)

Acute medications may include IV push Vasotec, The Angiotensin-Converting Enzyme Inhibitors or ACE inhibitors and ARBs suppress the renin angiotensin system (RAS) response to decreased renal blood flow. ACE inhibitors prevent conversion of angiotensin I to angiotensin II resulting in arterial dilation and increased stroke volume24Treatment of Heart FailureHuman B-type natriuretic peptides Nesiritide (Natrecor)Nitrates nitroglycerineInotropics digoxin increases contractility, reduces heart rate, slows condution through AV node, sympathetic activity parasympathetic activity Beta adrenergic agonists: Dobutamine (Dobutrex) milrinone (Primacor) acute treatment, both given IVBeta-adrenergic blockers not for acute treatment used for chronic treatment: carvedilol (Coreg), metoprolol (Lopressor), bisoprolol (Zebeta)Morphine for anxiety

Slide 25Vasodilator (recombinant DNA biosynthetic)Loading dose of 2 mcg/kg over approximately 60 seconds, followed immediately by continuous infusion of 0.01 mcg/kg per minute for 48 hrsNitrates: vasodilators venous and arteriole; side effects hypotension, headache, tolerance25Slide 26Hemodynamic RegulationInterventions:Reduce afterload.Reduce preload.Improve cardiac muscle contractility.Administer drugs as prescribed.Monitor for therapeutic and adverse effects.Teach client and family drug therapy.Preload and AfterloadPreloadis the end diastolic pressure that stretches the right or left ventricleof theheartto its greatest dimensions under variable physiologic demand, the initial stretching of the cardiomyocytesprior to contraction Afterloadis the tension or stress developed in the wall of theleft ventricleduring ejection. The end load against which the heart contracts to eject blood.Slide 27

Drugs That Reduce AfterloadAngiotensin-converting enzyme (ACE) inhibitorsperindopril,captopril,enalapril, lisinopril, andramipril. Relaxes blood vessels, as well as a decreased blood volume, lowers blood pressureand decreased oxygenSlide 28

Drugs That Reduce AfterloadHuman B-type natriuretic peptidesthe effect of BNP and Atrial natriuretic peptide (ANP) causes a decrease in blood volume, which lowers systemic blood pressure and afterload, yielding an increase in cardiac output, partly due to a higherejection fraction.Example: Nesiritide (Natrecor) for acute heart failure is only administeredintravenously by bolus then an infusion Slide 29Slide 30Interventions That Reduce PreloadDiet therapy: Patients should be given a low sodium diet to minimize fluid retention. Closely monitor fluid balance, fluid restrictionOxygen therapy to maintain SaO2 above 90 percentDrug therapy DiureticsVenous vasodilatorsSlide 31Drugs That Enhance ContractilityDigitalisDigitalis toxicity includes anorexia, fatigue, changes in mental status.Monitor heart rate and electrolytes.Inotropic drugs including dobutamine and milrinoneBeta-adrenergic blockers carvedilol (Coreg), metoprolol (Lopressor) 31S&PSlide 32Potential for Pulmonary EdemaPulmonary Edema Interventions:Assess for early signs, such as crackles, dyspnea at rest, disorientation, and confusion.Rapid-acting diuretics such as Lasix or Bumex.Oxygen is always usedStrictly monitor fluid intake and output.32Sentences and phraseSlide 33Infective EndocarditisInfective EndocarditisMicrobial infection involving the endocardiumOccurs primarily with IV drug abuse, valvular replacements, systemic infections, or structural cardiac defectsPossible ports of entry: mouth, skin rash, lesion, abscess, infections, surgery, or invasive procedures including IV line placementSlide 34Infective Endocarditis: Manifestations Infective EndocarditisMurmurHeart failureArterial embolizationSplenic infarctionNeurologic changesPetechiaeSplinter hemorrhages

Slide 35Infective Endocarditis: Interventions AntimicrobialsRest, balanced with activitySupportive therapy for heart failureAnticoagulantsSurgical management Slide 36Pericarditis Inflammation of the pericardiumDresslers syndromePost-pericardiotomy syndromeChronic constrictive pericarditis

Dresslers syndrome Post myocardial infarction pericarditis, 2-5 weeks after MI, was 2-3 percent now fewer cases due to current managementThe pain is the main symptom, often in the left shoulder, often pleuritic, and worse on lying down.There may be malaise, fever and dyspnea. Rarely, it may cause cardiac tamponade or acute pneumonitis.A pericardial friction rub may be heard. The typical sound of pericarditis is described as like the sound of boots walking over fresh snow.

36Slide 37Assessment Substernal precordial pain radiating to left side of the neck, shoulder, or backGrating, oppressive pain, aggravated by breathing, coughing, swallowingPain worsened by the supine position; relieved when the client sits up and leans forwardPericardial friction rub: two pieces of leather rubbing together, boots on snow37Sentences and phrasesSlide 38Interventions Hospitalization for diagnostic evaluation, observation for complications, and symptom reliefNon-steroidal anti-inflammatory drugsCorticosteroid therapyComfortable position, usually sittingPericardial drainage(Continued)38Sentence and phrases