Structural, Infectious, and Inflammatory Cardiac Disorders

Structural, Infectious, and Inflammatory Cardiac Disorders
And Complication of Heart Disease Updated Spring 14

What we will cover: Valvular diseases Cardiomyopathies
Inflammatory disorders Myocardial infarctions Some treatments

Pathophysiology Valvular stenosis: heart valves cannot open fully
Valvular insufficiency or regurgitation: heart valves cannot close completely Prolapse: valve stretches and balloons back into the atrium Acquired valvular disease occurs more frequently on the left side of the heart.

Valvular Heart Disease: Assessment
Grading Heart Murmurs Grade I: very faint Grade II: Faint, but recognizable Grade III: Loud, but moderate in intensity Grade IV: Loud, accompanied by palpable thrill Grade V: Very loud, accompanied by palpable thrill Grade VI: extremely loud, may be heard without stethoscope, accompanied by palpable thrill

Valvular Disorders Tricuspid Valve Mitral Valve Pulmonic Valve
Right Atrium from Right Ventricle Mitral Valve Left Atrium from Left Ventricle Pulmonic Valve Right Ventricle and Pulmonary Artery Aortic Valve Left Ventricle and Aorta Regurgitation Stenosis Prolapse

Mitral Valve Prolapse Causes Pathophysiology
Rheumatic disease Atherosclerosis Calcification Congenital Pathophysiology “redundancy of valve tissue; creates bulging, pulling away from other leaflet, allows regurgitation In severe cases of classic MVP, complications include Mitral regurgitation, infective endocarditis, and — in rare circumstances — cardiac arrest usually resulting in sudden death.

Mitral Valve Prolapse Often no symptoms; Rarely progresses, can result in sudden death More frequent in women than men Leaflet balloons back into Atrium during systole Open during ventricular contraction Blood regurgitates from left ventricle back into left atrium Symptoms: fatigue; dizziness, syncope; palpitations; chest pain; anxiety “Mitral Click” (systolic click) may be ausculatated

Mitral Valve Prolapse: Assessment
Manifestations related to Regurgitation of blood back into the Left atrium Usually asymptomatic S/S Fatigue, SOB, syncope CP, palpitations Mitral click, murmur

Mitral Valve Prolapse: Treatment
Prophylactic Antibiotic Therapy, before any operation that involves massive bleeding.

Mitral Valve Prolapse Management: controlling symptoms; eliminate caffeine, alcohol, smoking; antiarrhythmics, for chest pain: nitrates, calcium channel blockers or beta-blockers Nursing: education, prophylactic antibiotics before procedures, avoid caffeine, alcohol, tobacco; ephedrine; know epinephrine may produce dysrhythmias, avoid certain OTC meds Nurse explores diet, activity, sleep, other lifestyles Dysrhythmias, chest pain, heart failure could ensue

Mitral Regurgitation Causes Pathophysiology Rheumatic heart disease
Papillary muscle dysfunction or rupture Infective endocarditis Congenital anomalies Pathophysiology Incomplete closure allows the backflow of blood from L ventricle into L atrium L atrium & R ventricle dilate and hypertrophy

Mitral Regurgitation: Assessment
Fatigue, chronic weakness DOE, orthopnea, cough Palpitations, chest pain, A-fib Neck vein distention, Hepatomegaly, pitting edema High pitched S3 systolic apex Manifestations r/t L atrium can no longer respond to  blood flow Eventual R sided heart failure occurs

Mitral Regurgitation Problem with the chordae tendineae, annulus or papillary muscles holding the leaflets; may shorten or tear, calcify, rupture, stretch or pulled out of position From scarring from a MI Blood flowing back from left ventricle into left atrium during systole causing regurgitation of blood back into atrium during systole stretching left atrium eventually making it hypertrophy and dilate Diminishing volume of blood flowing into the atrium from the lungs

Mitral Regurgitation Lungs become congested eventually adding extra strain to the right ventricle Manifests itself with severe congestive heart failure, dyspnea, fatigue, weakness, palpitations, SOB on exertion, cough from pulmonary congestion Systolic murmur-high pitched, blowing sound at apex May be regular or irregular pulse Echocardiogram to diagnose and monitor progression

Mitral Regurgitation Management: CHF, MVR or valvuloplasy
Afterload reduction (arterial dilation) ACE-I Captopril (Capoten) Enalapril (Vasotec) Lisinopril (Prinivil, Zesteril) Ramipril (Altase) Hydralazine (Apresoline) Heart failure develops Restrict activity Antibiotic prophylaxis-prevent endocarditis Surgical Intervention Mitral valvuloplasy MVR

Mitral Stenosis Obstruction of blood flowing from left atrium into left ventricle Often caused by rheumatic endocardiitis which thickens valve leaflets, fusing them together, narrowing the orifice and obstructing flow into ventricle Backward flow from the atrium causes pulmonary circulation to become congested, resulting in right ventricle needing to contract against a higher pulmonary arterial pressure, eventually, the right ventricle fails First symptom is breathing difficulty (DOE) from pulmonary venous hypertension

Mitral Stenosis Causes Pathophysiology
Rheumatic carditis r/t rheumatic fever Calcium accumulation Thrombus formation Atrial myxoma Pathophysiology Valve leaflets fuse and become stiff, chordea tendineae contract and shorten Narrowing prevents blood flow from L atrium to L ventricle

Mitral Stenosis: Assessment
Manifestations r/t L atrial pressure , L atrium dilates, PAP , R ventricle hypertrophies Pulmonary congestion, R heart failure initially, eventually preload , cardiac output falls

Mitral Stenosis: Assessment
Fatigue DOE, orthopnea, paroxysmal nocturnal dyspnea, Hemoptysis, pulmonary edema, freq. respiratory infections Hepatomegaly, neck vein distention, pitting edema A-fib, apical diastolic murmur

Mitral Stenosis May have hemoptysis, cough, repeated respiratory infections Weak pulse, often irregular; low-pitched, rumbling diastolic murmur heard in apex Increased blood flow and pressure makes atrium dilate, hypertrophy and become electrically unstable (atrial dysrhythmias) EKG and cardiac catheterization determines severity Management: antibiotic prophylaxis to prevent recurrence of infections, treat CHF symptoms, anticoagulants to decrease risk of developing atrial thrombus, treatment of anemia Valvuloplasty, percutaneous Transluminal valvuloplasy or MVR

Aortic Regurgitation Flow of blood back into the left ventricle during diastole, caused by inflammatory lesions that deform leaflets of AV, preventing them from closing completely Caused by endocarditis, congenital abnormalities, syphilis, dissecting aneurysm that dilates and tears ascending aorta, or deterioration of an AVR Blood from aorta returns to left ventricle during diastole; LV dilates, hypertrophies, raising systolic BP. Arteries attempt to compensate by reflex vasodilation; peripheral arterioles relax, reducing peripheral resistance and diastolic BP.

Aortic Regurgitation Causes Pathophysiology Infective endocarditis
Hypertension Congenital Pathophysiology Aortic valve does not close completely Blood regurgitated from aorta back into L ventricle

Aortic Regurgitation: Assessment
Manifestations Related to: L ventricular hypertrophy due to dilation to accommodate greater volume L ventricular failure

Aortic Regurgitation: Assessment
S/S as disease progresses DOE, orthopnea, paroxysmal nocturnal dyspnea Palpitations with L side lying, nocturnal angina Nocturnal diaphoresis Bounding pulse, elevated systolic, diminished diastolic High pitch, blowing diastolic murmur

Aortic Regurgitation “forceful heartbeat” in head or neck, marked visible or palpable carotid or temporal arterial pulsations from, increasing force of increased blood ejecting from hypertrophied LV Progressive S/S of LV failure include: breathing difficulties (orthopnea, PND) Diastolic murmur heard as a high-pitched, blowing sound at third or fourth intercostal space, left sternal border occurs

Aortic Regurgitation Widened pulse pressure; WATER-HAMMER pulse (quick, sharp stroke then gone) Echocardiogram, radionuclide imaging, EKG, MRI, cardiac catheterization Management: antibiotics for procedures Heart failure and dysrhythmias; AVR before LVH

Aortic Stenosis Narrowing of the orifice between LV and Aorta from congenital leaflet malformation or abnormal number of leaflets; may be a result of rheumatic endocarditis or cusp calcification; Leaflets may fuse Over period of time, several decades LV overcomes obstruction to circulation by contracting more slowly but with greater than normal, resulting in thickening wall (remodeling)

Aortic Stenosis: Assessment
Exertional dyspnea Angina Syncope, fatigue Orthopnea, paroxysmal nocturnal dyspnea Systolic crescendo-decrescendo murmur Vibration felt over base of heart

Aortic Stenosis: Assessment
Manifestations related to: Ventricular hypertrophy Eventually L ventricle fails causing R sided heart failure

Aortic Stenosis Exertional dyspnea, dizziness, syncopy, angina BP low to normal, low pulse pressure Loud, rough systolic murmur heard over aortic area; crescendo-decrescendo murmur may radiate into carotid arteries and to apex of left ventricle, rough, rasping, vibrating

Aortic Stenosis Vibration palpated- turbulent blood flow across narrowed valve orifice 12-lead EKG and echocardiogram shows LVH Echo used to monitor progression, left-sided heart catheterization to measure severity (pressures) Antibiotic prophylaxis to prevent endocarditis Medication to control LVF and dysrhythmias AVR Symptomatic patients not good surgical candidates Balloon percutaneous valvuloplasy Nursing: education

Valve Repair / Replacement
Valvuloplasy Repair of cardiac valve Commissurotomy Open Closed Balloon Valvuloplasy Annuloplasty Leaflet Repair Chordoplasty

Surgical incision at the site where the leaflets meet (commissure) to relieve constriction of the mitral valve

Balloon Valvuloplasy For mitral stenosis in younger population
A balloon-tipped catheter is used to widen and separate stenotic valve flaps.

Annuloplasty (“tummy tuck”)
repairing the fibrous tissue at the base of the heart valve (the annulus). Sometimes, the annulus becomes enlarged, which enables blood to back up into the atrium. To repair this, sutures are sewn around the ring to make the opening smaller. This creates a purse string effect around the base of the valve and helps the leaflets meet again when the valve closes.

Annuloplasty (“support bra”)
Sometimes when repairing the annulus, it is necessary for the surgeon to implant an Annuloplasty ring. A ring is used to correct a problem, provide support for the valve, and reinforce other repair techniques or any combination of these.

Leaflet Repair

Valve Repair / Replacement
Types of Valve Prostheses Mechanical Tissue or biologic valves Xenografts Homografts Autografts Septal Repair Nursing management ICU nursing

Cardiomyopathy A condition in which a ventricle has become enlarged, thickened and / or stiffened Results in heart’s inability to be an effective pump

Cardiomyopathies Heart muscle disease associated with cardiac dysfunction Dilated Hypertrophic Restrictive or constrictive Unclassified Ischemic

Cardiomyopathies Arrhythmogenic right ventricular cardiomyopathy
Unclassified Manifestations May be without symptoms for years DOE, fatigue, orthopnea, PND, cough Pain, palpitations, dizziness, nausea, syncope with exertion, sudden death

Cardiomyopathies Review!!! Assessment What is JVD?
Crackles, JVD, pitting edema, enlarged liver Echocardiogram, EKG changes Chest x-ray Cardiac catheterization Review!!! What is JVD? Patient positioned under 45°, and the filling level of the jugular vein determined. In healthy people, it is maximum several (3-4) centimeters above the sternal angle.

Cardiomyopathies Management Underlying cause Low-sodium diet
Exercise-rest regimen Meds to control dysrhythmias Implantable cardioverter-defibrillator Fluid restriction LVAD Left ventricular outflow tract surgery Transplantation

Heart Transplantation
Techniques Heterotropic transplantation Postoperative Course

Mechanical Assist Devices and Total Artificial Hearts
Ventricular Assist Devices Total Artificial Hearts

complications may include:
Bleeding Blood clots Infection Device failure Adverse reaction to the anesthesia Kidney, lung, or heart damage

Nursing of Cardiomyopathy Patients
Assessment Detailed history Review of Systems Physical assessment Vital signs, pulse pressure, weight, PMI, heart tones, pulmonary sounds, JVD, Identification of presence and severity of edema

Nursing Diagnoses Decreased cardiac output Ineffective cardiopulmonary, cerebral, peripheral, and renal tissue perfusion Impaired gas exchange Activity intolerance Anxiety Powerlessness Noncompliance with medication and diet therapies

Collaborative problems or potential complications CHF Ventricular dysrhythmias Atrial dysrhythmias Cardiac conduction defects Pulmonary or cerebral embolism Valvular dysfunction

Nursing Interventions Improving cardiac output Rest Positioning Oxygen Medications Diet education Weight surveillance Monitoring for symptoms Skin breakdown

Physical Assessment Vital signs Calculation of pulse pressure and Identifying pulsus paradoxus Weight Detection by palpation of PMI; often shifted to the left Cardiac auscultation for a systolic murmur and S3, S4 Pulmonary auscultation for crackles Measurement of JVD Assessment of edema and its severity

Just to review: What is a pulse pressure? the change in blood pressure seen during a contraction of the heart the systolic pressure minus the diastolic pressure What is pulsus paradoxus? is an exaggeration of the normal variation in the pulse during respiration, in which the pulse becomes weaker as one inhales and stronger as one exhales An inspiratory fall in systolic arterial pressure of more than 10 mm Hg

Reducing anxiety Spiritual, emotional, psychological support Identify stressors Appropriate information Atmosphere changes Providing realistic hope Donors Help family anticipate grief

Decreasing sense of powerlessness Grieving process Loss of certain foods, life style, sports Identify emotional responses to loss Help with food selections Alternatives to improved sense of well-being (alternate activities)

Promoting home and community-based care Teaching self care and Continuing care Maintains and improves cardiac function Reports dyspnea, etc. Carries out ADLs Reports increased tolerance to activity Less anxious Adheres to diet Takes all meds as prescribed

Evaluation Expected patient outcomes Maintains or improves cardiac function Maintains or increases activity tolerance Is less anxious Decreases sense of powerlessness Adheres to self-care program

Infectious Diseases of the Heart
Rheumatic Endocarditis an inflammation of the endocardium (inside lining of the heart chambers and heart valves). Streptococcus infection Recognizing and preventing Rheumatic fever Pathophysiology Hemolytic streptococci Leukocytes Inflammatory response Damaged valve

Infectious Diseases of the Heart Rheumatic Endocarditis
Clinical Manifestations Leakage (regurgitation) Assessment Left-sided heart failure Prevention Prophylaxis for high risk patients symptoms

Manifestations Vegetation on valve flaps Gradual thickening of leaflets Few become seriously ill enough to require ICU As long as myocardium can compensate, patient remains in good health Unable to compensate, signs and symptoms of heart failure ensue

Assessment and diagnostic procedures Symptoms depend on side of heart involved Mitral valve Most affected Producing LEFT SIDED heart failure Shortness of Breath; crackles; wheezing At risk for embolism of lung, kidney, spleen, heart, brain, or peripheral vessels

Prevention Early recognition and adequate treatment of Streptococcal infections S/S of Streptococcal pharyngitis (high fever, chills, sore throat, redness of the throat with exudate, enlarged lymph nodes, abdominal pain, acute rhinitis

Rheumatic Endocarditis Management Eradicate causative agent Prevent additional complications Thrombotic event Long-term antibiotic (Penicilliin) Nursing Management Teach patient about disease Teach treatment Preventive steps Teach about antibiotics

Infective Endocarditis Infection of valves and endothelial surface of heart Usually in people with current structural defects (valve disorders) Older people (decreased immune system) IV drug abusers have higher incidence Caused by direct invasion of endocardium by microbe (the “ococci”s) causes deformities of the valves Higher risk in those with prosthetic valve, rheumatic heart disease, MVP, people with implanted grafts, long term indwelling catheters, immunosuppressed, cardiomyopathy

Infective Endocarditis Clinical Manifestations Onset usually insidious S/S develop from toxic effect of infection, destruction of valves, embolization of vegetative fragments S/S similar from rheumatic endocarditis

Infective Endocarditis
Assessment and Diagnostic findings Initially mistaken for flu Splinter hemorrhages Petechiae Osler’s nodes Roth’s spots Heart murmurs Enlarged heart CNS manifestations Embolic phenomenon may occur Blood cultures Echocardiogram shows mass on valve or other structures and development of heart failure

Infective Endocarditis Prevention Rare, but could be life-threatening Antibiotics for those in high risk All kinds of invasive procedures or those that will cause bleeding Amoxicillin (2 g) before dental, oral, esophageal, respiratory procedures If allergic to PCN Avoid the “cillins”! Instead, clindamycin (Cleocin), cephalexin (Keflex), azithromycin (Zithromax) or clarithromycin (Biaxin) may be used

Infective Endocarditis Nursing Prevention Know allergic status Teach about specific antibiotic Assure good dental hygiene Increased vigilance with IV catheters Meticulous hand washing, site preparation and aseptic technique during insertion and maintenance procedures Remove all catheters no longer needed or function

Management Pharmacologic Therapy Antibiotic therapy parentrally to keep high serum levels to ensure eradication (PCN) In fungal endocarditis, Amphotericin B Usually deliver in the home Serum levels monitored Blood cultures Monitor patient’s temperature Monitor appetite, monitor fatigue Psychosocial support for confinement with restrictive IV therapy

Surgical Management Seriously damaged valves may need replacement Aortic and mitral valves for development of CHF Those that have serious embolic episode, uncontrolled infection, recurrent infection, fungal endocarditis Infected prosthetic valve

Nursing Management Monitor patient’s temperature throughout illness Heart sounds Monitor S/S of systemic embolization Monitors for S/S pulmonary infarction or infiltrates Assess S/S of organ damage (CVA, meningitis, heart failure, MI, glomerulonephritis, splenomegaly

Patient care directed toward management of infection Assess all invasive lines, wounds Need for prophylactic antibiotic Patients and family instructed about restrictions, medications, and S/S infection Home health nurses supervise and monitor IV antibiotic therapy, educate and support

Myocarditis Inflammation of the myocardium (attack myocytes)
Causes heart dilation, thrombi on heart wall (mural thrombi), infiltration of circulating blood cells around the coronary vessels, between muscle fibers, and degeneration of muscle fibers themselves Causative Agents: Coxsackievirus A and B Rickettsial, fungal, parasitic, protozoal, or spirochetal infection

Myocarditis Assessment and Diagnostic Findings
May not reveal any abnormalities May C/O Chest Pain May develop dysrhythmias suddenly May develop cardiac enlargement Faint heart sounds, gallop rhythm, systolic murmur

Myocarditis Prevention Immunizations Early treatment

Myocarditis Medical Management PCN for hemolytic streptococci
Bed rest to decrease cardiac workload and myocardial damage Activities limited for 6-month period or until heart size and function returns to normal Physical activity increased slowly Corticosteroids controversial NO NSAIDs or ASA during acute phase or in heart failure

Myocarditis What drug reverses Digoxin? Answer on last slide
Nursing Management Assess temperature CV assessment on S/S heart failure and dysrhythmias Continuous cardiac monitoring closely monitor digitalis level for toxicity (very sensitive) What drug reverses Digoxin? Answer on last slide Elastic compression stockings (TEDS) Passive and active exercises to prevent venous thrombosis from mural thrombi

Acute Pericarditis Loose visceral pericardium and dense parietal pericardium surround heart Pericardial space may contain up to 50ml normally Etiologies of acute pericarditis-viral, bacterial, fungal, malignancy, drugs, radiation, connective tissue disorder, uremia, myxedema, post-MI, or idiopathic

Pericarditis Infections Disorders of the connective tissue
SLE, RF,RA, polyarteritis Hypersensitivity states: immune reactions, med reactions, serum sickness Leads to fluid accumulation in sac; increased pressure, cardiac tamponade; constrictive Calcified; decreased C.O. Restricted diastolic filling, increased SVR, peripheral edema, hepatic failure

Pericarditis Inflammation of the pericardium Causes
MI, dissecting aneurysm, pleural and pulmonary disease (pneumonia) Neoplastic disease Radiation therapy Trauma Renal failure and uremia TB

Acute Pericarditis Clinical Features
Most common-sudden or gradual onset of sharp or stabbing pain with radiation to back, neck, L shoulder or arm Radiation to L trapezial ridge is distinguishing Pain more severe with lying supine and relieved with sitting Low grade fever, dyspnea and dysphagia Transient, intermittent friction rub

Pericarditis Clinical manifestations
Chest pain (beneath clavicle, neck, left scapula) Fairly constantly May worsens with deep inspiration and when lying down or turning Relieved with forward-leaning or sitting position Friction rub Increased WBC, increased ESR or SED rate Dyspnea, other signs of heart failure from pericardial compression due to constrictive pericarditis or cardiac tamponade

Pericarditis Assessment and Diagnostic Findings
Made on basis of the patient’s history, signs, and symptoms Echocardiogram may detect inflammation and fluid build-up Indications of heart failure 12-lead EKG detects ST changes

Acute Pericarditis Diagnosis
EKG-changes in four stages 1-ST elevation in I, V5 and V6, PR depression in II, aVF and V4-V6 2-ST segment normalizes, T wave decreases 3-Inverted T waves in leads with previous ST elevation 4-Return to normal ECG In I, V5, or V6 ST: Twave ratio >0.25 most likely acute pericarditis

Acute Pericarditis Diagnosis and Differential
Chest X-ray-normal and can help r/o other disease Other tests of value-CBC, BUN and CR, streptococcal serology, viral serologies, antinuclear/anti-DNA abs, thyroid function, ESR, Cardiac Enzymes

Acute Pericarditis ED Care and Disposition
Idiopathic or presumed viral etiology-outpatient with NSAIDs for 1-3 weeks Treat any indentified specific causes Admit for myocarditis or hemodynamic instability

Pericarditis Medical Management
Determine cause Administer therapy Be alert for cardiac tamponade Bedrest for impaired C.O. NSAIDs and ASA to relieve pain during acute phase Corticosteroids if severe or not responding to NSAIDs Colchicine (anti-inflammatory) Pericardiocentesis to remove fluid (relieves symptoms) Pericardial window allows continuous drainage Pericardietomy to release both ventricles from constrictive and restrictive inflammation

Pericarditis Nursing Management
Be alert to possibility of cardiac tamponade Falling arterial pressure Rising venous pressure Distant heart sounds Pain- requiring analgesic medication Positioning Psychological support (not heart attack!) Nurse educates

Pericarditis Assists with activity restrictions until pain gone
Nurse encourages gradual increases in activity as improvement Nurse educates patient and family about healthy lifestyle to enhance patient’s immune system Monitor for heart failure Hemodynamically unstable treated same as acute heart failure

Pericarditis Nursing Process Assessment
Pain (observing and evaluating in various positions Is pain influenced by respiratory movements? Is pain with flexion, extension, or rotation of spine? What precipitates or intensifies pain?

Pericarditis Nursing Process (continued) Assessment (continued)
Pericardial friction rub from loss of lubricating fluid because of inflammation LEFT STERNAL edge, 4th ICS Scratchy or leathery sound Rub louder at end of exhalation, heard best when leaning forward Rub is audible on auscultation; synchronous with heartbeat

Pericarditis Nursing Diagnosis Potential Problems Planning and Goals
Acute pain related to inflammation of the pericardium Potential Problems Pericardial effusion Cardiac tamponade Planning and Goals Relief of pain Absence of complications

Pericarditis Nursing Interventions Relieving Pain Patient rest
Sitting up or leaning forward relieves pain – positioning (chair rest) Restrict activity until pain subsides As chest pain and friction rub abate, ADL resume Responses to medications (corticosteroids, analgesics, antibiotics)

Nursing Monitoring Pericardial Effusion Cardiac Tamponade
Fluid accumulate between pericardial sac or linings Can constrict myocardium and interrupt ability to pump Decreased C.O. Cardiac Tamponade Falling arterial pressure, JVD Systolic pressure falls while diastolic pressure remains stable (narrowing pulse pressure) Notify MD, assist with pericardiocentesis Stay with patient and continuous assessment, monitoring, recording signs and symptoms, intervene to decrease patient’s anxiety

Evaluation Expected Outcomes Absence of complications Free of pain
Performs ADL without pain, fatigue, SOB Temperature returns to normal No pericardial friction rub Absence of complications Sustains BP in normal range Heart sounds strong and can be auscultated No JVD

Cardiovascular Emergencies

Cardiogenic Shock Heart can’t pump enough blood to supply amount of oxygen needed by the tissues S/S r/t tissue hypoperfusion Cerebral hypoxia: restlessness, confusion, agitation  B/P, rapid/weak pulse Cold/clammy skin BS, urinary output Dysrhythmias

Cardiogenic Shock: Management
PAC monitoring Correct underlying problem MI Dysrhythmias Hypervolemia or hypovolemia Rest Treat hypoxemia: O2, intubation with sedation

Cardiogenic Shock: Management
Pharmacological: based on CO, MAP Vasopressors: norepinephrine (Levophed), dopamine (Intropin) Diuretics, vasodilators: used carefully to reduce workload Non-pharmacological Intra-aortic balloon pump (IABP) Internal counterpulsations to augment pumping action of the heart

Pericardial Effusion and Cardiac Tamponade
Pericardial effusion: accumulation of fluid in pericardial sac. R/T: pericarditis, advanced HF, hemorrhage (surgical or trauma) Increased fluid raises pressure and compresses the heart (cardiac tamponade)  R&L ventricular end-diastolic pressure venous return Inadequate filling of ventricles

Pericardial Effusion and Cardiac Tamponade: Manifestations
Feeling of fullness in the chest Pain/pressure Engorged neck veins SOB, syncope, cough Pulsus paradoxus Distant (muffled heart sounds)  systolic B/P Treatment Pericardiocentesis

What do these meds do? You need to know….
ACE-Is AIIRBs Hydralazine and Isosorrbide Dinitrate (Apresoline, Isordil, Sorbitrate Beta blockers Diuretics Digitalis Calcium channel blockers

Nutritional Therapy Low sodium diet (2 to 3g/day)
More salt in canned (soups, bouillon) than in chips! Avoidance of excessive amounts of fluid (under 2,000cc/day) includes free water and food water Avoid grapefruit / grapefruit juice Fish Veggies Whole grains Avoid alcohol

Digoxin Toxicity Hold medication while monitoring for S/S
Cardiac signs include functional rhythms, heart blocks, ventricular rhythms, acute tachycardia, and bradycardia, anorexia, nausea, and vomiting Get digoxin level What is Therapeutic Dig level? Digoxin: range 0.5 to 1.9 ng /ml Reverse with Digibind Binds with Digoxin and makes it unavailable to the body Monitor Potassium level and renal function

Cardiac Compromise Chest pain results from ischemia.
Ischemic heart disease involves decreased blood flow to the heart. If blood flow is not restored, the tissue dies (infarct). Injury leads to inadequate heart function and death.

Chest Pain Pathophysiology
Mediastinum: Angina: stable or unstable AMI Esophagitis, esophageal rupture Pericarditis Mediastinal air Thoracic dissection Mitral valve prolapse

Chest Wall: Traumatic contusion/tamponade Cysts and infections Rib cartilage inflammation Shingles (Herpes Zoster) Muscle strain, overuse syndromes

Lungs and pleura: Pleurisy Pneumonia Pneumothorax, hemothorax Pulmonary embolus Asthma, bronchitis, URI

Abdomen: Gallbladder (cholecystitis, stones) Stomach (gastritis, GERD, perforated peptic ulcer) Pancreas (pancreatitis) Esophagitis, perforation

Chest Pain Psychogenic: Stress Hyperventilation
Anxiety and panic attacks

Classic Symptoms Pressure, fullness, heaviness, squeezing pain in center of chest with radiation Diaphoresis Nausea Shortness of breath Weakness

Frequency of Symptoms Diaphoresis 78% Chest pain 64% Nausea 52%
Shortness of breath 47% No signs/symptoms 25% N Engl J Med 1984;311:1144-7

Atypical Presentations
Common in the elderly, diabetics, and females: Unusual fatigue Sudden onset of unusual shortness of breath Nausea, dizziness Belching, burping, indigestion Palpitations, new dysrhythmia Pain only in jaw, neck, back, arm

All chest pain is considered to be an AMI until proven otherwise!

Angina Pectoris Chest pain caused when heart tissues do not get enough oxygen for a brief period of time. Typically crushing or squeezing. Onset with the 3-E’s. Usually resolves with rest or meds. May be difficult to diagnose from AMI Angina occurs when a person with atherosclerosis exerts or is stressed. The heart muscle does not receive adequate blood flow and thus it becomes ischemic. Anaerobic metabolism begins and produces lactic acid and CO2 which accumulates in the myocardium causing pain. This process usually does not happen when the patient is at rest. 3-E’s: Exercise, eating, and emotion. Anginal pain that is not typical of normal angina or relieved by rest and meds indicates possible unstable angina.

Acute Coronary Syndrome
Used to describe the range of conditions from unstable angina to AMI. Signs and symptoms usually caused by acute myocardial ischemia.

ACS Signs & Symptoms Shortness of breath Signs of inadequate perfusion
Chest pain, pressure, or discomfort (with or without radiation to back, neck, jaw, arm, wrists) Nausea Weakness/syncope Dysrhythmias

Acute Myocardial Infarct
Usually caused by the same mechanism as angina only with resulting tissue death. Time is myocardium: Consequences can be serious: Congestive heart failure Cardiogenic shock Sudden death

Acute Anterior MI Primary Rapid assessment of chest pain patient
Correct EKG interpretation Initiation of therapy (ASA, NTG, beta blockers) Definitive therapy (interventionalist vs. lytics and anticoagulation)

Acute Anterior MI Secondary Risk factor assessment
Pain scale to guide response to therapy Ensure adequate access, appropriate monitoring Informs patients and families Seeks contraindications to lysis (if lytics used)

Acute Anterior MI Critical Actions Checklist Chest Pain Evaluation
Rapid H+P, early EKG, CXR IV access, blood for cardiac enzymes, CBC, chemistries) Cardiac monitor, pulse oximeter

Acute Anterior MI Recognition of Acute Anterior MI EKG interpretation
Compare to previous EKG Treatment Initiation Aspirin Nitroglycerin Beta blockers Anticoagulation Morphine

Acute Anterior MI Rapid Definitive Therapy (Interventional vs. Thrombolytics) Failure to obtain or correctly interpret EKG Awaiting labs for treatment Delaying definitive treatment

Cardiogenic Shock Heart lacks power to force blood through the circulatory system. Brought on when 40% of left ventricle is infarcted. Onset may be immediate or not apparent for 24 hours. Cardiogenic shock is due to the impaired ability of the heart to pump. It can be caused by disorders of the heart muscle, the valves, or the heart’s electrical conduction system with AMI being the most common cause. Dead myocardium does not contract, therefore, a weakened heart cannot pump enough blood throughout the body. There is an adequate blood volume but failure to blood in circulation. Hypoxia results due to inadequate perfusion.

Signs & Symptoms Altered LOC Rapid, shallow breathing
Restlessness and anxiousness Pale, cool skin Tachycardia/dysrhythmia Hypotension

Congestive Heart Failure
Occurs when the ventricles are damaged. Heart tries to compensate with increased heart rate. Enlarged, ineffective left ventricle Fluid builds up into lungs or body as “pump” fails. AMI damages left ventricle. A weakened left ventricle is unable to pump blood effectively throughout the body. The blood and fluid backs up into the pulmonary veins and lungs. This fluid in the lungs reduces gaseous exchange in the alveoli (pulmonary edema). Hypoxia results due to inadequate oxygenation of the blood.

Signs & Symptoms Fatigue Cough with pink, frothy sputum
Dypsnea, tachypnea Pulmonary edema Agitation and confusion Hypertension Pedal edema, ascities

Signs & Symptoms Sudden and severe chest or upper back discomfort. “Pain shoots to the shoulder blades.” Anxiety Diaphoresis Nausea

Cardiac Tamponade Trauma induced, filling of the pericardial sac with blood. Signs of shock JVD Decrease pulse pressures

Esophageal Rupture Usually underlying alcohol abuse. Shock signs.
Coughing up bright red blood.

Pericarditis Inflammation of the pericardium caused by infection.
Usually presents as sharp discomfort. Changes with breathing and movement.

Chest Pain Assessment BSI/Scene Safety Initial Assessment (Sick/Not Sick) Focused Exam Detailed Exam Assessment Treatment and Plan

Initial Assessment 60second clinical picture to determine if Sick or Not Sick (Oxygen) Based upon your initial impression: Body position skin signs and color respiratory rate and effort mental status pulse rate and character Correct immediate life threats!

Focused Exam (S) Your subjective findings are based upon what the patient or historian tells you: Patient Age Sex Chief Complaint LISTEN TO THE PATIENT!

Focused Exam (S) SAMPLE History
Signs/Symptoms (associated with cardiac chest pain): Diaphoresis (78%) Shortness of Breath (47%) Pain/discomfort (64%) Nausea/vomiting (52%) No signs or symptoms (25%) N Eng Journal Med 1984;311:

Focused Exam (S) Onset – Provocation – Quality –
“When and at what time did it start” Provocation – “Does anything make it better or worse?” “Does it change with position, palpitation, inspiration?” Quality – “Describe the pain/discomfort in your own words”

Focused Exam (S) Region/Radiation – Severity – Time –
“Where does it start?” “Does it radiate anywhere?” Severity – “On a scale of 1 to 10, what was the pain/discomfort at onset?” “What is the pain/discomfort at now?’ Time – “When did this episode start?” “How long has it been going on?”

Focused Exam (S) Allergies Medications – Past Medical History –
Cardiac meds = cardiac problems. Ask about OTC meds, natural supplements, vitamins? Past Medical History – “Do you have any cardiac history?” “Risk factors such as smoking, diabetes, HTN, weight/diet?””

Focused Exam (S) Last Oral Intake Events Leading to Call –
“What were you doing when this event started?” Think activity induce vs. non activity

…they will tell you exactly what is wrong!
Listen to the patient… …they will tell you exactly what is wrong!

Focused Exam (O) Objective findings from your physical exam of the patient. Look for evidence of trauma/injury Evaluate: Level of consciousness Skin color and temperature Respiratory rate and effort Pupillary reaction Pulse rate Blood pressure (bilateral for chest pain!)

Focused Exam (O) Listen to breath sounds Palpate chest Palpate abdomen
Check pedal pulses BGL if diabetic with DLOC SpO2 after BP, confirm with pulses, RA & after administration of O2 Rhythm strip?

Focused Exam (O) Based upon your clinical findings
Observe the patient while they are talking with you, note any distress/discomfort (Levine sign) Watch for acute clinical signs: jugular vein distension, tracheal deviation, paradoxial chest movement.

Detailed Exam (O) Complete and thorough neck, head to toe examination with non-critical patients if needed or time permits. Elicit further information and necessary interventions. Key in on critical findings!

Assessment (A) This is your best guess (or rule out) as to what is going on with the patient. It is based upon YOUR Subjective and Objective findings and should help you develop and implement your Plan for patient care.

Plan (P) Medics? ABC’s/Monitor vitals Patient in position of comfort.
Oxygen via ? Assist with medications. Maintain body temperature. Calm and reassure. Minimize patient movement. Rapid transport!

Other Stuff Coronary artery bypass graft (CABG) and other open heart surgeries Percutaneous transluminal coronary angioplasty (PTCA) Automatic implantable cardiac defibrillators (ACID) Pacemakers

Structural, Infectious, and Inflammatory Cardiac Disorders

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Structural, Infectious, and Inflammatory Cardiac Disorders

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