7/23/2016

A. Acute Coronary Syndrome B. Dysrhythmias C. Failure D. Other Cardiac Issues ◦ Papillary Muscle Rupture ◦ Ventricular Septal Rupture ◦ Ventricular Aneurysm Cheryl Herrmann, APN, CCRN, CCNS-CSC-CMC ◦ ◦ Acute Inflammatory Disease E. Vascular Issues

CMC CSC

} Located in the ventricles } Three papillary muscles in RV ◦ Anterior -- largest ◦ Posterior ◦ Septal } Two papillary muscles in LV ◦ Anterior -- largest ◦ Posterior } Attached to the AV valves (mitral & tricuspid) } Contact to prevent inversion or prolapse of the mitral or triscuspid valves } Prevents regurgitation

www.online-nursing-dot.com

Cause Clinical Manifestations

} Complication of AMI } ↑ RAP, PAP, PAOP } Hypotension } Occurs within first } Large v waves on } week PAOP waveform } Dyspnea ↓ } More with inferior MI } CO/CI } Crackles ↓ or subendocardial MI } SpO 2, SvO 2 } S3 } New holosystolic at the apex

Symptoms of Acute Cardiogenic & Pulmonary Congestion New holosystolic at the apex

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Cause Treatment

} Complication AMI } Prepare for emergency replacement } Occurs 3 and 5 – 7 } Treat the symptoms of the mitral regurgitation, days post AMI and pulmonary congestion } Complication of ◦ Supportive management until surgery ◦ Afterload reduction with nitrates and nitroprusside ◦ Diuretics ◦ IABP ◦ Oxygen/ventilator

Treatment } Hypotension } ↑ RAP, PAP } Tachycardia } Large v on PAOP } Emergent surgical repair } Tachypnea waveform } Supportive care of cardiogenic shock while } ↑ SvO } New holosystolic 2 ↑ preparing for surgery murmur at lower left } oxygen gradient (left to right shunt) ◦ Vasodilators sternal border ◦ Inotropes } Inaccurate ↑ CO/CI } Thrill ◦ Diuretics ◦ IABP } Pulmonary congestion } Syncope

Sudden hemodynamic compromise and pulmonary congestion New holosystolic murmur at lower left sternal border

} Opening of the septum between the right and left Clinical features } Oxygenated in the } Harsh and loud holoystolic LV returns to the RV murmur rather than the } Left atrial dilation } Left ventricular enlargement oxygenated blood } Pulmonary dilation continuing forward to } Left to right shunt deliver oxygen to the Normal Heart & Heart with VSD cells. Normal Heart & Heart with VSD } Results in an increase in ventricular workload } Leads to heart failure Holosystolic murmur

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Clinical Presentation } A ballooning, dyskinetic area of infarcted myocardium } Diffuse PMI – spread over more than one ICS } Left ventricular heave } May be a complication } Atrial Fibrillation or ventricular arrhythmias of AMI } Persistent ST segment elevation } Prone to dysrhythmias, } CXR= left ventricular dilation intraventricular } Echo = dyskinesia and left ventricular dilation thrombus formation, } Signs of LVF may be present and rupture } Systemic emboli symptoms may be present ◦ Cerebral emboli ◦ Peripheral emboli with acute arterial occlusion

Treatment } Mitral } Aortic Medical } Antiarrhythmic medications } Possible ablation for ventricular arrhythmias } Anticoagulation medications } Treatment of HF with ACEI, beta blockers, diuretics, inotropes, and vasodilators

Surgical } Excision of the weakened area of the myocardium, } Patch is sewn in the edges of the remaining viable myocardium

} An acquired or congenital disorder of a cardiac Common Causes of Acquired valve Valvular heart disease } Characterized by ◦ Stenosis (obstruction) } Rheumatic heart disease ◦ Regurgitation (backward flow) } Degenerative diseases } Can occur acutely } Infective endocarditis } Typically is a chronic progressive disorder } Causes a significant impact on quality of life } Medical management delays the inevitable surgery for replacement/repair } Prosthetic valve creates new problems

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Clinical Management } Large anterior leaflet

} Cardiac compensatory mechanisms can maintain } Small posterior stability for years before symptoms occur. leaflet } Key is early diagnosis to prevent the long-term consequences } Chordae tendineae ◦ Pulmonary hypertension and papillary ◦ Heart Failure muscles prevent the ◦ Atrial fibrillation ◦ Thromboembolism prolapse of valve } Important to understand leaflets into left ◦ The structure and function of the valves during ◦ The causes and treatments of each disorder systole

} Mitral valve will not } Cause Pathophysiology open completely ◦ Mostly 1. Small opening causes } Restricts flow of ↓ ↓ ◦ Some calcified blood flow and CO ↑ blood from left degenerative disease 2. workload in Left Atrium atrium to LV 3. ↑ pressure in LA } Continuous, slow 4. LA dilation & hypertrophy progressive disease 5. May lead to A fib with symptoms 6. LA blood flow stagnant appearing 20-40 7. May cause clot formation & thromboembolism years after 8. ↑ in LA pressure ‰backflow into pulmonary artery rheumatic fever 9. Leads to pulmonary hypertension, congestion, right ventricular hypertrophy and right sided heart failure

LV size and contractility = normal in MS

} Ruddy face (mitral facies) Clinical Presentation } } Nx LV function ◦ Loud first heart sound S1 (closing snap) } Pulmonary Hypertension } Mild MS ◦ Mid-diastolic murmur/rumble ◦ Dyspnea on exertion from at apex } RV failure pulmonary congestion ◦ Opening snap ◦ Right sided S3 & S4 } Tricuspid insufficiency } Moderate MS ◦ Right ventricular heave at ◦ Fatigue sternum } High left atrial pressures and pulmonary } CXR ◦ Paroxysmal nocturnal ◦ Left atrial and RV enlargement pressures dyspnea ◦ Pulmonary congestion ◦ Atrial fib } EKG } Low CO and pulmonary congestion ◦ LA enlargement: Notched P } Severe MS waves P Mitrale ◦ Dyspnea on mild exertion ◦ Right ventricular hypertrophy or at rest – tall R waves V 1 & V2

Pulmonary congestion & right sided failure signs

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} Causes } Assess for pulmonary hypertension } Mitral valve fails to ◦ Anything that affects any } Increased PVR leads to RV failure close completely part of the MV } Increased CVP = possible RV decompression ñ Mitral annulus } TEE to assess for RV and LV function } Blood is propelled ñ Valve leaflets } Dobutamine, Milrinone, Norepinephrine to increase backward into the LA ñ Chord tendineae ñ Papillary muscle contractility of RV and $ PVR during systole } Fluid administration ◦ Mitral Valve Prolapse } PAD does not reflect LA filling pressures related to pulmonary ◦ Rheumatic heart disease hypertension – Wedge more accurate ◦ Infective endocarditis } PA catheter may be placed farther in related to dilated ◦ Cardiomyopathy pulmonary ◦ Ischemic heart disease } IABP usually not indicated as no LV dysfunction but RV ◦ dysfunction

Pathophysiology } Heart Sounds Clinical Presentation ◦ Holosystolic murmur – high pitched, blowing at apex ◦ S2 – widely split 1. During systole, a portion of blood is ejected } May be asymptomatic ◦ Displaced PMI laterally back into the LA for years ◦ Maybe right sided S3 & S4 ↓ ↓ } CXR 2. blood in LV ‰ CO } Initial symptoms ◦ Cardiomegaly 3. ↑ blood in LA ‰ ↑ LA pressures ‰ pulmonary ◦ Left sided failure ◦ LA enlargement ↑ ‰ ◦ LV hypertrophy congestion and pulmonary pressures RV ◦ Dyspnea on exertion ◦ Possible pulmonary hypertrophy } Cough congestion } EKG 4. During diastole, blood continues to flow into } Peripheral Edema ◦ LA enlargement P mitrale ↑ LV ‰ LV volume } from new ◦ Left and/or right ventricular hypertrophy 5. LV hypertrophy onset of A fib ñ Large QRS complexes

MR = LA enlargement, Left or Ventricular Failure Endocarditis risk is RARE

} Mitral valve leaflets } Cause: myxomatous } Immediate # SVR due to no backflow of blood prolapse back into degeneration of valve in LA leaflets causes the left atrium during } Pulmonary hypertension & Myocardial leaflets to enlarge systole hibernation take time to reverse and prolapse } Inotropes (Milrinone, Dobutamine) } Frequently asymptomatic & no } IABP treatment needed } Monitor for RV failure } Midsystolic click } Late systolic murmur

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} Repair preserves native valve } Has three leaflets or } Repair is favored due to disadvantages of cusps prosthetic valves } Cusps close as the ◦ No anticoagulation needed for repair pressure in the aorta } Technically more difficult becomes greater ◦ Depends on degree of regurgitation, than the pressure in ◦ Pathophysiology of the regurgitation the left ventricle. ◦ LV function, ◦ Ability of surgeon

} will not } Most common valve Clinical Presentation open completely lesion in USA ◦ Echocardiogram: } Restricts flow of } Gradual progressive disease – usually ñ Grades: blood from left ñ Normal AVA > 2.5 – 3.5 ventricle to aorta remain cm2 asymptomatic for ñ Mild AVA > 1.5 cm2 ñ Moderate AVA = 1.0 – 1.5 decades. cm2 ñ Severe AVA < 1.0 cm2 ñ Critical AVA < 0.75 cm2 ñ Mean gradients: > 40-45 mmHg ñ Peak velocity over 4 m/s

Syncope --- Systolic ejection harsh murmur

Pathophysiology Clinical Presentation } Heart Sounds ◦ Systolic ejection murmur (harsh) at the right 1. Small opening causes ↓ blood flow and ↓ CO } Syncope, Dyspnea, sternal border radiating to neck 2. ↑ Afterload , – especially } CXR 3. ↑ workload in Left ventricle with exertion ◦ May be normal 4. ↑ pressure in LV } Angina more common } EKG 5. LV hypertrophy if CAD as comorbidity ◦ Left ventricular 6. LV becomes stiff } HF with severe AS hypertrophy with severe 7. High LV pressures leads to LV failure AS and left atrial enlargement ◦ Left Atrial enlargement, 8. High pressures transmitted to the Left axis deviation, Left lungs leads to pulmonary BBB hypertension, pulmonary edema and right sided failure LV size and contractility = abnormal in AS Syncope --- Systolic ejection harsh murmur

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} Causes } Inotropes rarely needed } Aortic valve fails to ◦ Pathological conditions of the aortic valve cusps or ◦ Except in patient with impaired LV function – may close completely aortic root. be caused by myocardial stunning ◦ Valve cusps } Backflow of blood ñ Rheumatic heat disease } Avoid ↑ BP in immediate post-op period into the left ventricle ñ Infective endocarditis ◦ “thin” aorta in bicuspid valve patients– more likely to rupture during diastole ◦ Aortic Root under high pressure ñ Hypertension } Maintain AV Synchrony ñ Aortic dissection ñ Marfan’s Syndrome } Maintain adequate preload ñ Syphilis ñ PCWP > 15 mm HG ◦ Severe AI – most frequently caused by } Avoid and inotropes bicuspid valve ◦

Pathophysiology } Due to dilated ventricle use

1. Volume overload leads to compensatory mechanisms ◦ IV vasodilators ◦ Left ventricular hypertrophy ◦ Inotropic support to promote ventricular empting ◦ ↑ End-diastolic volume which allows normal EF despite ↑ afterload. ñ Milrinone 2. ↑ LV afterload as the ↑ volume ejected into the high ñ Dobutamine pressured aorta. ◦ IABP 3. Ventricular wall thickening with dilatation to accommodate volume overload. } Maintain AV synchrony 4. Ventricular wall thickens without enlargement but with diminished capacity to accommodate pressure overload. 5. The balance between afterload excess, preload reserve, and hypertrophy may continue for decades 6. Symptoms occur when this balance can’t be maintained and there is a reduction in EF or LV dysfunction AI – unique with both volume & pressure overload

} Aortic Valve Replacement (mainstay) } Trileaflet bioprosthesis mounted on a balloon catheter delivered through the arterial system via a } Aortic Valve Repair (not mainstream) guidewire. Device is inserted into the midpoint of the } Transcatheter Aortic Valve Replacement native valve (TVAR)

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Pro’s } Less invasive than traditional AVR’s } No sternotomy or cardiopulmonary bypass } Femoral most } Less ventilation time or extubated in OR common } Shorter ICU length of stay and often discharged within 48 hours postop

Con’s } Elderly population with comorbidities } Higher risk for delirium due to sedation or pain management } Screening for physical therapy

https://www.youtube.com/watch?v=ztl3cc2EOmM

} Exclusionary Criteria: ◦ Bicuspid or unicuspid or noncalcified aortic valve } Indications ◦ Native aortic annulus size <18 mm (for a native valve), and no greater than 29 mm – size ◦ Severe symptomatic aortic stenosis not amenable/too high risk for dependent (4 sizes available currently) open AVR ◦ Severe native aortic regurgitation (>3+) ñ >50% mortality } Relative Exclusion Criteria: ñ NYHA class II or greater ◦ Evidence of MI within 1 month of valve placement ◦ Hemodynamic or respiratory instability requiring inotropic support, mechanical ventilation, or ñ 1 cardiologist and 2 surgeons mechanical heart assistance within 30 days ◦ Life expectancy greater than 1 year ◦ Hypertrophic cardiomyopathy with or without obstruction ◦ Aortic annulus by CT and echo appropriate size ◦ Left ventricular ejection fraction <20 percent ◦ Porcelain aorta ◦ Severe pulmonary hypertension and right ventricular dysfunction ◦ Frailty ◦ A known contraindication or hypersensitivity to all anticoagulation regimens or inability to be anticoagulated for the study procedure ◦ Chest deformity - radiation ñ Dual antiplatelet therapy is required for at least 3 months ◦ Open bypass grafts ◦ Renal insufficiency (eg, creatinine >3.0 mg/dL) and/or end-stage renal disease requiring ◦ Liver cirrhosis chronic dialysis ◦ Pulmonary fibrosis ◦ Echocardiographic evidence of intracardiac mass, thrombus, or vegetation ◦ Magnetic resonance imaging-confirmed stroke or transient ischemic attack within six months ◦ Impaired LV function (180 days) of the procedure. ◦ Renal disease ◦ Severe incapacitating dementia ◦ Estimated life expectancy <12 months due to noncardiac comorbid conditions ◦ Severe mitral regurgitation ◦ Significant aortic disease, including the following abnormalities may preclude a transfemoral approach: ñ Could be done transaortic or transapical

‹ Usually extubated in OR, if not within 2-4 hrs postop ‹ Monitor hemodynamics, neuro assessment, urine ‹ Monitor bilateral puncture sites – hold pressure if oozing or bleeding output, & chest drainage same as an open ‹ Monitor distal to insertion site due to the large sternotomy incision catheters and embolization risk ‹ Wean to extubate within 6 hours of anesthesia ‹ Monitor neuro assessment due to high risk for strokes end time. Encourage incentive spirometer every ‹ Maintain SBP between 100mmHg – 130mmHg hour while awake • May use beta blockers or other vasodilators for hypertension ‹ Discontinue femoral lines after extubation ‹ Discontinue Arterial line after extubation and venous ‹ Ice chips and advance diet as tolerated sheath when ACT < 180 ‹ Up in chair early am and ambulate with physical ‹ Internal Jugular discontinued on POD 1 and transferred to Telemetry therapy or nurses 3-4 times/day ‹ ‹ All patients assessed for rehab upon transfer from ICU Discontinue PA catheter and arterial line POD 1 V

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} Causes } Complete Heart Block due to Aortic Valve edema. } Aortic valve fails to ◦ Pathological conditions of } Hypotension the aortic valve cusps or ◦ Monitor amount of sedation or vasodilating medications for close completely aortic root. cause of hypotension ◦ Valve cusps } Backflow of blood ñ Rheumatic heat disease } Check groin sites for bleeding, lower abdomen for into the left ventricle ñ Infective endocarditis signs of retroperitoneal bleed, check peripheral during diastole ◦ Aortic Root vascular pulses ñ Hypertension ñ Aortic dissection } Monitor Labs (Hgb/Ht) ñ Marfan’s Syndrome } Vasovagal response ñ Syphilis ◦ Severe AI – most } Stroke frequently caused by - Assess neuro status with VS’s bicuspid valve ◦

Pathophysiology Clinical Presentation } Heart Sounds ◦ Decrescendo diastolic blowing murmur – best 1. Volume overload leads to compensatory mechanisms ◦ Left ventricular hypertrophy } May be asymptomatic heard in upright position ◦ ↑ End-diastolic volume which allows normal EF despite ↑ afterload. for years and leaning forward. 2. ↑ LV afterload as the ↑ volume ejected into the high } CXR pressured aorta. } Fatigue ◦ Enlarged heart 3. Eccentric hypertrophy (ventricular wall thickening with dilatation) to accommodate volume overload. } Dyspnea on exertion ◦ Dilation of proximal aorta 4. Modest concentric hypertrophy (ventricular wall thickens } Angina } EKG without enlargement but with diminished capacity) to accommodate pressure overload. } Palpitations ◦ Left ventricular 5. The balance between afterload excess, preload reserve, and hypertrophy hypertrophy may continue for decades } Widen pressure 6. Symptoms occur when this balance can’t be maintained and > 50 mmHG there is a reduction in EF or LV dysfunction

AI – unique with both volume & pressure overload Wide pulse pressure – Diastolic blowing murmur

Clinical Presentation } Rheumatic Signs } Endocarditis (esp IV drug abuser)

} Austin Flint murmur } Functional (most common form): secondary ◦ Decrescendo diastolic blowing murmur to left sided pathology often accompanied by } Hill Sign ◦ Systolic BP in lower extremities at least 20mmHg higher than pulm HTN arms } Duroziez sign } Congenital: AV canal, VSD, Ebsteins, Myxoma ◦ Systolic and diastolic heard when femoral artery is compressed by stethoscope } Corrigan pulse ◦ ↑ volume and rate of the rise of the radial pulse when the wrist is elevated perpendicular to the body of a supine patient } de Musset sign ◦ Bobbing of the head with each systolic beat

https://www.youtube.com/watch?v=C6mTmpP9Lvw

9 7/23/2016

} Primary indication for tricuspid valve repair is Tissue Mechanical severe TR in patients requiring surgery for mitral valve disease Age Over65 yo Under 65

} Tricuspid stenosis: don’t see often Longevity 10-15 years Potentially Lifetime } TR: with left sided lesion, right sided failure, Anticoagulation Aspirin lifelong Warfarin lifelong mod to severe TR Warfarin – 3 months??? Reoperation risk Patient dependent As low as 1% risk lifetime

} AHA/ACC Guidelines: ◦ Mechanical prosthesis: } Physical examination ñ Already have a mechanical valve in the mitral or tricuspid ◦ Normal prosthetic heart valve sounds: position ñ Mechanical valves: ◦ Bioprosthesis aka “Tissue” valve: ñ Loud, high-frequency, metallic closing sound ñ Any age who will not take warfarin or who have major medical contraindications to warfarin therapy ñ Soft opening sound ñ Aged 65 years or older without risk factors for ñ Tissue valves: thromboembolism ñ Closing similar to those of native valves ñ Woman of childbearing age ◦ New onset murmurs is a concern ◦ Homograft: ñ murmur – though hard to hear – would raise ñ Active prosthetic valve endocarditis suspicion ◦ TAVI/TAVR: ñ High prohibitive risk for open AVR per FDA guidelines ñ Moderate risk: Partner II trial

} Embolic complications } Prosthetic heart valve malfunction: ◦ Stroke ◦ Acute prosthetic valve failure: ◦ TIA ñ Sudden onset of dyspnea, syncope, or precordial pain } Anticoagulant-related hemorrhage ñ Sudden death ◦ Hemorrhage site – brain, abdomen, etc. ñ Hyperdynamic precordium } Dysrhythmia ñ Pronounced JVD ◦ AV Block ◦ Subacute valve failure: ◦ Atrial dysrhythmias ñ Gradually worsening congestive heart failure ñ Unstable angina ñ Hemolytic anemia ñ Asymptomatic

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} Blood borne bacterial traveling to the heart and growing on the valve } He is discharged on POD # 3 } Dental or other procedures may provoke bacteremia } His post op recovery for the next 8 weeks is unremarkable. } Went to dentist for dental cleaning six days ago

} BP 137/80 } A few days ago he began feeling very tired, his pulse was irregular } HR 98 } RR 18 } Went to ED in rural hospital } T 100.9 Orally } Atrial Fibrillation Rate 140 } SpO2 97% } Given Lopressor 5 mg IV } Transferred to referral hospital

} Clindamycin 600 mg prior to cleaning (Allergic to PCN) } Echodense mobile structure on the } Started experiencing diarrhea the next two posterior leaflet suggestive of infective days so took Imodium endocarditis close to the annular ring on the posterior leaflet without signs of } Diarrhea subsided now (three days later) abscess

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} Antibiotic prophylaxis is indicated for the following high-risk cardiac conditions: ◦ Prosthetic cardiac valve ◦ History of infective endocarditis ◦ Congenital heart disease (CHD) ◦ Cardiac transplantation recipients with cardiac valvular disease } For these procedures ◦ Dental ◦ Invasive respiratory (bronch)

} Amoxicillin } Medical therapy is first line treatment ◦ Adult dose: 2 g PO } Surgery indicated for those patients with ◦ Pediatric dose: 50 mg/kg PO; not to exceed 2 acute infective valve endocarditis and life- g/dose threatening heart failure or cardiogenic shock ◦ Administer once as a single dose 30-60 min before the procedure. } Ampicillin, Clindamycin, Cephalexin, Cefazolin, or Ceftriazone ◦ May be used if allergic or unable to take oral ◦ See guidelines for specific doses

1. Aortic Stenosis 1. . 2. 2. . 3. Mitral Stenosis 3. Mitral Stenosis 4. Mitral Regurgitation

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MS MR AS AR/AI

Heart MS MR AS AR/AI Sounds Heart Mid diastolic Holosystolic Systolic Decrescendo Sounds murmur at murmur high ejection diastolic blowing Symptoms the apex pitched murmur harsh murmur – best heard sitting S3, S4 Widely at right upright RV heave S3, S4 sternal border Symptoms Dyspnea Peripheral Syncope Fatigue Pulmonary edema Dyspnea Dyspnea Hypertension Cough Angina Angina Palpitations Pulmonary LV failure Wide pulse symptoms New onset pressure > 50 Atrial size AFib mmHG } Austin Flint murmur Ventricular } Hill Sign Size } Duroziez sign } Corrigan pulse } de Musset sign Atrial size LA enlarged LA enlarged LA enlarged LA enlarged

Ventricular LV normal LV enlarged LV enlarged LV enlarged Size

Mitral Stenosis Mitral Regurgitation Preop Nx LV function Enlarged left atrium Aortic Stenosis Aortic Regurgitation Pulmonary Hypertension Both common to have atrial RV failure fibrillation Preop LV hypertrophy LV hypertrophy High atrial & pulmonary ↑ SVR pressures s/s heart failure Pulmonary congestion

Post op LV may not IV vasodilators to ↓ SVR Post op Assess pulmonary Immediate # SVR due to no anticipate ↓ in SVR Inotropic support to hypertension (PVR) backflow of blood in LA Dobutamine or Milrinone Pulmonary hypertension & and continue to promote empting LV: + Norepinephrine to ↑ myocardial hibernation take pump hard Milrinone/Dobutamine contractility of RV & ↓ time to reverse Avoid hypertension IABP PVR Inotropes (Milrinone, Fluids Dobutamine) + epinephrine and stress on suture ↑ CVP may indicate RV IABP line decompression Monitor for RV failure Treat atrial fibrillation Treat atrial fibrillation

} Inflammation of the heart muscle } Challenging to diagnose and treat

Myocarditis Endocarditis Pericarditis

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} Immune Mediated Causes ◦ Allergens Phases } Subacute: Day 4 – 14 ◦ Alloantigens ◦ Infiltrating mononuclear ◦ Autoantigens cells } Infectious ñ Chagas Disease } Acute: Day 0 – 3 ◦ Cytokine production ◦ Bacterial ñ Systemic lupus ◦ T and B lymphocytes ◦ Spirochetal ñ Sarcoidosis ◦ Viral infection activated ◦ Fungal ◦ Myocyte change ◦ Neutralizing antibodies } Toxic Myocarditis ◦ Protozoal ◦ Drugs ◦ Myocyte antigens ◦ Viral clearance ◦ Parasitic ñ Amphetamines released } Chronic myocarditis: Day ◦ Rickettsial ñ Anthracyclines ◦ Cytokines released ◦ Viral ñ Cocaine 15 – 90 ñ Ethanol ñ Coxsackievirus ◦ Fibrosis ◦ Heavy metals ñ Human immunodeficiency virus ◦ Cardiac enlargement ñ Copper ◦ Apoptosis ñ Iron ñ Lead ◦ Physical agents ñ Electrical shock ñ Radiation

Source: Moser & Riegal. Cardiac Nursing 2008

} Heart Sounds ◦ Distant Clinical Presentation ◦ S3 or S4 Treatment ◦ } EKG } Supportive management of } Observe for pericarditis and } History of recent flu-like ◦ Ventricular Arrhythmias ◦ Heart Block HF symptoms tamponade symptoms ◦ IABP ◦ Fever ◦ Diffuse ST segment changes } Bedrest due to increased and T wave changes ◦ VAD ◦ Arthralgia (joint pain) } CXR } risk of myocardial ◦ Fatigue Treat cause Cardiomegaly inflammation ◦ ◦ ◦ Antibiotics ◦ Pulmonary congestion ◦ Antifungals } Advise to abstain from } Labs ◦ Pleural or ◦ Antivirals ↑ exercise for several months ◦ Troponin I ◦ Corticosteroids ↑ ◦ CK MB ◦ Withdrawal of offending agent } Close and consitent follow- ◦ ↑ ERS } Endomyocardial biopsy for } Anticoagulation if AF up every 1 – 3 months ◦ Leukocytosis definitive diagnosis ◦ Cardiac immunoglobulin } Early consideration for ◦ Persistent inflammation will antibody titer 1:40 or greater transplant if: lead to dilated ◦ Progressive HF cardiomyopathy ◦ Giant cell myocarditis Wide variance in symptoms – minimal symptoms to fulminant Heart Failure

} Inflammation/infection of the Causes or lining of the heart. } Usually involves the membrane } IV drug use lining the heart valves } Body piercing } The invading pathogen typically adheres to the heart valves } Dental procedures } The pathogen creates solid } Poor oral hygiene vegetation or masses of bacteria, WBC, platelets, and } Rheumatic fever fibrin that invade and destroy } Invasive procedures surrounding tissues } Affects aortic and mitral valves more than tricuspid

Most common bacterial pathogens are Staphylococcus and Streptococcus and fungal pathogens Aspergillus fumigatus and Candida albicans

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Acute infective High risk groups endocarditis Subacute endocarditis

} Valve repair or replacement patients } Progresses rapidly } Manifests initially as flu-like } Often caused by symptoms and progresses } Patients with invasive lines Staphylococcus infection slowly and prolonged ◦ Central lines course ◦ Pacemakers } Typically occurs with } Often caused by ◦ Cardiac caths normal valves and causes severe damage to the valves Streptococcus or gram } Hemodialysis patients negative infection } Congenital or acquired valvular heart disease } Typically occurs with ◦ Septal defects already damaged valves ◦ Bicuspid aortic valve } Outcome is usually good ◦ Mitral valve prolapse with adequate treatment } Immunosuppressed state

Clinical Presentation Diagnosis

} May be nonspecific } Labs } Echocardiogram ◦ Fever } Embolic or allergic ◦ Diaphoresis vasculitis signs ◦ Positive blood cultures ◦ Intracardiac vegetation ◦ Weight loss ◦ Osler’s nodes: painful ◦ ↑ ERS ◦ Dysfunctional valves ◦ Myalgia (muscle pain) nodules on pads of fingers ◦ Night sweats ◦ Anemia or and toes ◦ Leukosytosis ◦ Janeway lesions: nontender } Overt complications ◦ ↑ C-reactive protein ◦ Embolic stroke macules on palms and soles ◦ Heart failure ◦ Roth’s spots: round white ◦ Abnormal urinalysis } Heart sounds lesions on the retina ◦ ↑ WBC ◦ New or changed murmur ◦ Occur from ◦ S3 microembolization of the ◦ Pericardial friction rub original vegetation

Complications Treatment

} Acute Renal Failure } Antimicrobial therapy } CVA } Eradiation of endocardial vegetations } Conduction Abnormalities } Long term IV bacterial antibiotics } Heart Failure } Supportive therapy to treat and prevent } Mycotic aneurysm complications from the disease progression } Paravalvular abscess, perforation, or fistula } If not responsive to medical therapy, surgery } Pericarditis may be an option ◦ Valve repair/replacement } Pulmonary emboli ◦ Optimal time for surgery is when the patient is } Septic arthritis hemodynamical stable } Splenic abscess/infarct

} Systemic embolization Source: Moser & Riegal. Cardiac Nursing 2008

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Prophylaxis } Two days ago noticed abdomen and back } Prevention is essential in high risk groups were swollen. It was difficult to feel his } Prophylactic Antibiotics ◦ Dental, oral, upper respiratory tract procedures spine as there was so much fluid ñ Amoxicillin } ñ Ampicillin Unable to walk across the room without ñ Clindamycin becoming SOB ñ Azithromycin ñ Cephalexin } Breathing worse when lying flat ñ Cefazolin ◦ Genitourinary or gastrointestinal procedures } Difficulty speaking in full sentence ñ Amoxicillin ñ Ampicillin } Dry cough ñ Vancomycin } Weight gain of 10 pounds in last week } Avoid unnecessary invasive lines } “Don’t Do Drugs!” } Avoid body piercing

} BP 140/90 } Recent admission five days ago for } HR 109 hematuria, hyperkalemia, and acute renal insufficiency } RR 24, moderately labored } Left ureteral stent placed for sever } T 98.7 hydrohephrosis of the left kidney } SpO 2 97% on 3 liters nasal cannula } Received 2 units of blood at that time } Weight 66.2 kg } Pansystolic murmur 4/6 noted loudest at the left sternal border } Coarse rales throughout all lung fields

• One pack a day smoker • Rarely drinks • Occasional use of marijuana • Has tried cocaine, Ecstasy, Adderall in the past • Had several tattoos done a few months ago.

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} Given Lasix with 1300 ml urine output in ED } Started on Rocephin and Azithromycin • Procalcitonin 0.14 (normal) } Plan for echocardiogram • Urine toxicology (with earlier admission) – Positive for methamphetamines and cannabinoids • DAU-12 – Positive for benzodiazepines and THC (marijuana) • BNP 5002

ó Severely dilated left ventricular chamber ó EF 50 – 55% ó Normal LV systolic function. Abnormal LV diastolic function ó LV filling diastolic filling pattern is restrictive ó Thickened bicuspid aortic valve which probably is sessile vegetation. ó Freely mobile vegetation in the LV outflow tract ó Moderate to severe aortic insufficiency ó Moderate mitral insufficiency ó Mild tricuspid regurgitation ó Small circumferential pericardial effusion ó Severe pulmonary hypertension ó Left atrium moderately dilated ó Right atrium mild to moderately dilated

Diagnosis } Streptococcus viridans aortic valve and infectious endocarditis ó Acute congestive heart ó Diurese failure ó Start lisinopril } Changed antibiotics to ceftriaxone ó Bacterial endocarditis of ó Cardiothoracic surgery } PICC line placed. Ceftriaxone 2 grams IV the aortic valve and consult every 24 hours for 6 weeks. probable mitral ó Infectious disease involvement consult ó Bicuspid aortic valve ó Admits to Heroin and ó Pericardial effusion LSD ó Mild renal insufficiency

17 7/23/2016

} The organisms are most abundant in the mouth, and one } Aortic Valve Replacement with #23 Trifecta member of the group, S. mutans , is the etiologic agent of dental caries. Others may be involved in other mouth or Valve gingival infections. } If they are introduced into the bloodstream, they have the potential of causing endocarditis, particularly in individuals with damaged heart valves. They are the most common causes of subacute bacterial endocarditis. } Viridans streptococci have the unique ability to synthesize dextrans from glucose, which allows them to adhere to fibrin-platelet aggregates at damaged heart valves. This mechanism underlies their ability to cause subacute valvular heart disease following their introduction into the bloodstream (e.g., following tooth extraction).

Source: Wikipedia. August 29, 2011

} https://www.youtube.com/watch?v=Q6sRyrB_UMA } Inflammation of the pericardial sac } Inflammation may cause fluid leak into the pericardial space ◦ Tamponade is possible ◦ Constrictive pericarditis ñ Scarring, thickening and fibrous of the

Causes Clinical Presentation } Dyspnea* } Can mimic AMI ◦ Unrelated to exertion } Numerous causes } Complication after AMI ◦ Chest pain ◦ Caused by the inability to take ◦ ST segment elevation deep breaths } Viral – most common } Metastasis ◦ Esp in lung cancer (30 %) ◦ Have patient point to the exact } Pericardial friction rub } Idiopathic location of the pain } Radiation induced ◦ Heard best left lower sternal } Complication of HIV-AIDS – } Pleuritic chest pain border, 4t or 5 th ICS pericarditis ◦ Persistent, sharp, stabbing TB pericarditis ◦ To heard best, pt should lean } Uremic pericarditis- chronic ◦ Aggravated by inspiration and } Bacterial renal failure coughing forward so the pericardium is ◦ Stab wound } Medications ◦ Localized to the retrosternal and closer to the chest wall ◦ Cardiac surgery ◦ Procainamide left pericardium } Chills/Fever – may be ñ With deep inspiration the ◦ Pneumonia ◦ Hydralazine diaphragm pulls on the inflamed antecedent ◦ INH (isoniazid) pericardium causing the sharp } SOB/Cough ◦ Endocarditis pain that radiates } Weakness } Fungal – more common in ◦ Pain is worse when recumbent immunosuppressed people ◦ Pain maybe relieved by sitting upright and leaning forward Pain when recumbent ñ Mohammed’s Sign Dyspnea unrelated to exertion

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Clinical presentation Diagnostics

} LABs } as } 12 Lead EKG – most evidenced by definitive diagnostic test ◦ Troponin, CK negative ◦ True dyspnea and SOB ◦ ↑ WBC, Sed rate, C- } CXR – may have enlarged ◦ Pulmonary congestion reactive protein ◦ ↓ CO cardiac silhouette (water ◦ Positive blood cultues if ◦ Decreased tissue perfusion bottle heart) ◦ Pericardial knock due to infection ñ High pitched, sharp, early } Echo diastolic sound heard best ◦ Possibly Pericardial at lower LSB with patient leaning forward effusion ◦ PAP > 50 mmHG ◦ Pericardial thickening with constrictive pericarditis Muffled heart sounds = tamponade Pericardial knock = constrictive pericarditis

Acute: Pericardial Chronic: inflammatory response Dressler syndrome

} Pericarditis occurring } Autoimmune response 2 – 7 days after AMI to myocardial necrosis } Related to the } Involves both the inflammation and pleura and pericardium healing process } Occurs 2 – 4 weeks to several months post AMI } Diffuse ST elevation } Scooping upwardly concave ST segment elevation in almost all leads except AVR } No reciprocal ST depression except in AVR } PR depression

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} Accumulation of Clinical Management excessive fluid in the pericardial sac } Relieve pain } Pericarditis after AMI } Sac normally holds 15 – ◦ NSAIDs ◦ NO corticosteroids or ◦ Indomethacin & colchicines anti-inflammatory agents 50 ml of fluid – for intolerance to NSAIDs } When excessive ◦ If unresponsive to NSAIDS ñ Can cause rupture of the infarcted area ñ Narcotic analgesia accumulation is slow, the ñ Short course of } Pericardiocentesis for pericardium can stretch. corticosteroids tamponade } Cardiac tamponade } Treat cause } Pericardial window for occurs when the ◦ Antibiotics if bacterial recurrent effusion pericardium cannot } If anticoagulants are given, assess for } Pericardiectomy – stretch to accommodate tamponade constrictive pericarditis the excess fluid

} Cardiomyopathy --- will see the pulmonary hiatus (vasculature)

} Pericardial Effusion } Water bottle 11 } (Above) 11 7 8

Causes

} Initial causes of pericarditis } Blunt or penetrating chest trauma } Malignancy or radiation } Retrograde extension of } Autoimmune disease aortic dissection } AMI } Iatrogenic causes } Complications of cardiac ◦ Myocardial perforation with surgery invasive lines (pacers, } Drugs central lines, angiogram) } Chronic renal failure on dialysis } Hypothyroidism } Heart failure

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Clinical Presentation } Rapid occurring } Slow occurring effusions effusions ◦ Accumulation of pericardial fluid or buildup of a ◦ Asymptomatic volume of pericardial fluid ◦ Often undetected as the exceeding the gradual stretching of pericardium’s ability to pericardium doesn’t expand compromise ventricular ◦ Leads to tamponade filling ◦ Compromises ventricular filling ◦ ↓ Cardiac output ◦ 100 – 200 ml of extra fluid can elevate pericardial } Compression of the heart due to collection pressure from 1 – 5 mmHg to 30 mmHg or greater. of fluid or blood in the pericardial space

Clinical Presentation

} Hypotension } Beck’s Triad } Low urine output ◦ Hypotension } Rising & equalization of CVP ◦ Neck distention & PAD ◦ Muffled heart sounds } Large a and v on PAOP “M”

} Falling SVO 2, CO/CI } Widening mediastinum on CXR } Cool extremities } Tachycardia } Pulses Paradox >10 mmHG ◦ ↓ in systolic BP with inspiration

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Clinical Management

} Closed Pericardiocentesis (preferred) } Open Surgical Pericardiocentesis ◦ Creation of a pericardial window to drain pericardium

Post pericardial window Pericardial Effusion for pericardial effusion

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Myocarditis Endocarditis Pericarditis Myocarditis Endocarditis Pericarditis

Definition Definition Inflammation of the Inflammation of Inflammation of heart muscle the lining and the pericardial sac valves Constrictive – signs of tamponade

Heart Sounds Heart Sounds Distant New or changed Pericardial friction S3, S4 murmur rub – Pericardial Pericardial friction rub S3 knock Pericardial rub best heard leaning forward

Symptoms Symptoms Wide variance from flu Embolic events Recumbent pain like to HF Osler’s nodes: Pleuritic chest pain Ventricular Janeway lesions: Can mimic AMI – arrhythmias/ blocks Roth’s spots: diffuse ST Â, no reciprocal or Q Bedrest– no exercise Prophylaxis waves for several months

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