CARDIAC NOTES

Anatomy and Physiology Heart Three layers Endocardium (Inner layer) Ex (endocarditis is inflammation of inner layer) Myocardium (middle layer /muscular lining) Epicardium/pericardium (outer layer/ sac) PericardiumThe pericardium has 2 layers filled w/ fluid. When it gets inflamed and filled w/ more fluid there is Pericardial friction rubIn order to distinguish a pericardial friction rub (heart) from pleural friction rub (lungs) need to ask pt to hold respiration for few seconds

Four chambers Heart valves Atrioventricular (A-V) valves (S1/SYSTOLE) Semilunar valves (S2/DIASTOLE) Coronary arteries (Feed the heart) Cardiac conduction system Cardiac hemodynamics (pressure of blood/ fluid volume status)Overview of Anatomy and Physiology Heart Cardiac Cycle Systole (contraction) Diastole (relaxation) Cardiac Output= HR X SVAnything that decrease cardiac output causes: dizziness, fatigue, LOC changes, shortness of breath HR SV Preload (diastole, relaxation, if there is a lot of fluid the preload will be increased and vice) Afterload (systole, contraction) Contractility Autonomic Nervous System (ANS) SNS (increase) PSNS (decrease)Terms - Cardiac Output Stroke volume: amount of blood ejected with each heartbeat Cardiac output: amount of blood pumped by ventricle in liters per minute Preload: degree of stretch of cardiac muscle fibers at end of diastole Contractility: ability of cardiac muscle to shorten in response to electrical impulse After load: resistance to ejection of blood from ventricle Ejection fraction: percent of end diastolic volume ejected with each heart beat

CO = SV x HRControl of heart rateAutonomic nervous system, baroreceptors (located in aortic arch, righ carotid, the monitor pressure throughout the body, when the pressure is low, they send a signal to speed the HR)Control of stroke volumePreload: Frank-Starling Law (AMOUNT THE HEART CAN STRETCH WHEN FILLING UP)After load: affected by systemic vascular resistance, pulmonary vascular resistanceContractility increased by catecholamines, SNS, some medications (Epinephrine, dopamine)Decreased by hypoxemia, acidosis, some medications

Cardiac Conduction SystemProperties of the conduction system: Automaticity (ability of stimulate on its own)ExcitabilityConductivitySinoatrial (SA) nodeInternodal pathwaysAtrioventricular (AV) nodeBundle of HisBundle BranchesPurkinje fibers

Terms - Cardiac Action PotentialDepolarization: electrical activation of cell caused by influx of sodium into cell while potassium exits cellRepolarization: return of cell to resting state caused by re-entry of potassium into cell while sodium exitsRefractory periodsEffective refractory period: phase in which cells are incapable of depolarizingRelative refractory period: phase in which cells require stronger-than-normal stimulus to depolarizeAssessmentHealth historyDemographic informationFamily/genetic history -CAD-DM (bc glucose damages the vessels, makes them hard, decrease blood flow, and perfusion)- HTNCultural/social factors (smoking, drinking, drugs, food)

Risk factorsModifiable (diet, weight, drugs, smoking, exercises, stress management)Nonmodifiable (age, gender, race, genetics)Most Common Clinical Manifestations (MI, ANGINA, HF) Chest pain (due to lack of O2, hypovolemia or low BP, can also cause chest pain) Dyspnea (difficulty breathing) Peripheral edema, weight gain (retention of H2O.) Fatigue (not enough O2, pt get tired) Dizziness, syncope, changes in level of consciousness Acute Coronary Syndrome (is prodromal, before, like S/S that there is a cardiac problem.-Shortness of breath-Swell feet- Tired Experience prodromal symptoms for a month to more prior to acute event

AssessmentMedicationsNutrition (Low Na, low cholesterol)Elimination (avoid straining, to avoid increase pressure)Activity, exerciseSleep, restSelf-perception, self-conceptRoles, relationshipsSexuality, reproductionCoping, stress tolerancePrevention strategies

Laboratory Tests Cardiac biomarkers Serum Enzymes:- Creatinine Kinase (CK), CK-MBWhenever there is injury to the heart muscle CK formerly known as (CPK)- elevation indicates muscle injury CK-MB: specific to myocardial muscle, rises within 6 hours of injury and peaks at 18 hours post injury and returns to normal within 2-3 days. Useful in DX of MI- Lactic dehydrogenase (LDH) After an MI, LDH is always elevated. THIS TEST IS DONE AFTER TROPONIN I, AND CK-MB Found in many body tissues; elevation is detected within 24-72 hours after MI,peaks in 3-4 days and returns to normal around 2 weeks. Useful for delayed DX of MI- Troponin T and I (First to be drawn, bc is more specific)Is released when there is damaged to cardiac muscle (is the most important to detect Heart attack, mainly Troponin I which is specific for heart muscle, troponin T is heart muscle and skeletal muscle) Onset is before CK-MB in MI; peaks at 24 hours and returns to normal around 2 weeks; provides early sensitivity More specific to cardiac injury for DX of MI

Laboratory TestsLipid profile: to determine risk factors of developing atherosclerosis (to determine what build up of plaque)Total serum lipids= 400-800 mg/dLTriglycerides: lipids stored in fat tissue; normal 100-200 mg/dLCholesterol: main lipid associated with CAD; normal < 200mg/dLLipoproteins: proteins in the blood to transport cholesterol, triglycerides and other fatsHDL= 35-70 mg/dL (M); 35-85 mg/dL (F)LDL= < 160 mg/dL

Laboratory TestsBrain (B-type) natriuretic peptide (BNP) BNP, is secreted from the ventricules, it indicates, INCREASED PRELOAD, TOO MUCH FLUID. IS TO RULE OUT CHF. If BNP is elevated then I need to look further for CHF.A neurohormone that helps regulate BP and fluid volume.Secreted from the ventricles in response to increased preload with elevated ventricular pressureUseful in the diagnosis of HFGreater than 100 pg/mLC-reactive protein (CRP)A protein produced by the liver in response to inflammation. It is not specific for heart. Anywhere where there is infection or injury to the body (Heart attack, plaque to heart, cut in the toe anything that causes damage in the body elevates this protein)

Elevated CRP is increased risk for CAD (Coronary Artery Disease)High: 3.0 mg/dl or greaterModerate: 1.0-3.0 mg/dLLow: less than 1.0 mg/dL

Laboratory TestsHomocysteine (not specific for heart attack)An amino acid linked to the development of atherosclerosis (deposit of plaque in arteries) because it can damage the endothelial lining of the arteries and cause thrombus formationA 12 hour fast is necessary before drawing a blood sample for an accurate serum measurementOptimal: less than 12 mol/LBorderline: 12-15 mol/LHigh risk: above 15 mol/L

Myoglobin (not a primary heart test)O2 binding protein found in heart and skeletal muscle. Found in the blood when released following muscle injury. Laboratory TestsCoagulation StudiesPartial thromboplastin time (PTT): 60-70 (Heparin)Activated partial thromboplastin time (APTT): 20-39 Prothrombin time (PT): 9.5-12 (Coumadin)International normalized ratio (INR); 2-3.5Hematologic StudiesComplete blood count (CBC)Hematocrit: M 42-52% F 35-47%Hemoglobin M 13-18 g/dL F 12-16 g/dLPlatelets: 150,000-450,000/ mmWhite Blood Cells (WBC)Drug LevelsDigoxin: Therapeutic range is 0.5-2 ng/mLDigoxin has a narrow therapeutic range. Drop blood levels routinelyQuinidine: Therapeutic range is 2-6 mcg/mLLaboratory TestsElectrolytes: normal levels are essential for proper cardiac functionPotassium (K): 3.5-5.0Hypo: ventricular dysrhythmias, flattened T wave or presence of U waveHyper: ventricular dysrhythmias, tall peaked T waves and asystoleSodium (Na): 135-145Hypo: intracellular osmotic fluid shift= brain edemaHyper: increased BP, abnormal HR, seizures, neurological impairmentCalcium (Ca):Low Ca = low HRHight Ca= tachycardia Hypo: ventricular dysrhythmias, prolonged QT interval, and cardiac arrestHyper: shorten the QT intervals and causes AV block, cardiac arrest

Magnesium (Mg):High Mg=BradycardiaLow Mg= Tachycardia Hypo: ventricular tachycardia and fibrillationHyper: bradycardia, hypotension, prolonged PR and QRS intervalsElectrocardiography12 lead ECGContinuous monitoring: hardwire, telemetrySignal-averaged electrocardiogramContinuous ambulatory monitoring (HOLTER)Transtelephonic monitoringWireless mobile monitoringCardiac stress testing Exercise stress testing (how heart work in stress, exercises)Pharmacologic stress testing (how pt response under certain meds)Diagnostic TestsRadionuclide imagingMyocardial perfusion imaging (if heart is perfussing well)Test of ventricular function, wall motionComputed tomography CT (Looking at structures)Positron emission tomographyMagnetic resonance angiographyDiagnostic TestsEchocardiography (ultrasound of the heart)US of heart to evaluate the structure and function of chambers and valvesPhonocardiography (recording w/ a simutaneos ECG)Graphic recording of heart sounds with simultaneous ECGCoronary Angiography/ArteriographyInvasive procedure where cardiologist injects dye into coronary arteries and immediately takes a series of x-ray films to assess structure of arteriesCardiac CatherizationInvasive procedure study used to measure cardiac chamber pressures, assess patency of coronary arteriesRequires ECG, hemodynamic monitoring; emergency equipment must be availableAssessment prior to test; allergies, blood work (PT, PTT)Assessment of patient post-procedure; circulation, potential for bleeding, potential for dysrhythmiasActivity restrictionsPatient education pre-, post-procedure

Hemodynamic Monitoring Central Venous Pressure (CVP) (volume status)High fluid or hypervolemia= Increased CVP and viceCVP is looking at the right side of the heart Appropriate for clients who require accurate monitoring of fluid volume status butare not candidates for the more invasive pulmonary artery pressure monitoring Done by a central catheter with the tip in the SVC to measure the R heart filling pressure Provides data about right ventricular preload. Not for left heart pressures Normal CVP 2-8 cm H2O or 2-6 mm Hg Decreased CVP= decreased circulating volume Increased CVP= increased blood volume or right heart failure

Diagnostic Tests Pulmonary artery pressure (PAP)PAP = left side of heart High PAP = TOO MUCH FLUID and vice Appropriate for critically ill clients requiring more accurate assessments of left heart pressures Pulmonary artery catheter (Swan-Ganz) has the tip in the pulmonary artery Pressure is obtained after the tip is wedged into a pulmonary capillary and is called PCWP Good indicator of left ventricular preload also called left ventricular end diastolic pressure (LVEDP)

Normal Values of Hemodynamic ReadingsDiagnostic TestsIntra-Arterial Blood Pressure MonitoringTo obtain direct and continuous BP measurements in critically ill patients who have sever hyper or hypertensionArterial catheters are useful when ABGs are needed frequentlyAllen test completed prior to insertion of catheter. Allen test is to check for perfusion in the hand-Ask pt to make a fist- Occlude both (ulnar and radial arteries)- Ask pt to open hand - Release ulnar artery and check for return of blood to hand (red/pink hand)

Common Cardiovascular MedicationsAce Inhibitors prilsAngiotensin Receptor Blockers sartansBeta Blockers: ololsCalcium Channel Blockers: dipineAdrenergic Agonists (EPINEPHRINE, DOBUTAMINE)Anticoagulants: Coumadin, HeparinCardiac Glycosides: Digoxin Antidysrhythmics (Lidocaine, Quinidine) to correct fast dysrhythmiasDiuretics (eliminate excess fluid)Antihyperlipedemia (niacin, statin, Lipitor)Thrombolytics (clot busters, but you have to have a clot to give this)Vasodilators (hydrolicine )Nitrates (vasodilation, for chest pain. Too much could aggravate angina due to decrease perfussion)Analgesics MorphineOxygenNytroglicerineAspirinPhysical Assessment-CardiacGeneral appearanceInspection of skinBlood PressureArterial pulsesJugular venous pulsationsHeart inspection and palpationHeart auscultationInspection of extremitiesAssessment of other systemsLungsAbdomenCardiac Assessment- Auscultation Normal Heart Sounds S1: Tricuspid and mitral closure creates first sound Heard the loudest at the apical S2: closure of the pulmonic and aortic valves Heard loudest over the aortic and pulmonic areas Abnormal Heart Sounds S3: heard after S2 Normal in children and adults up to 35 or 40 (physiological S3) Abnormally is due to overload of one or both ventricles (significant in HF) S4: heard before S1 Generated during atrial CX as blood forcefully enters a noncompliant ventricle Caused by ventricular hypertrophy: HTN, CAD, cardiomyopathy, etc.

Cardiac Assessment- AuscultationSystolic clicks:Caused by opening of rigid and calcified aortic or pulmonic valve duringventricular CXMurmurs: (due to valvular problems)Created by turbulent blood flowCauses of the turbulence may be a critically narrowed or malfunctioning valveFriction Rub: (two layer of pericardium friction together)Harsh grating sound that can be heard in both systole and diastole.Caused by abrasion or inflamed pericardial surfaces from pericarditis

Cardiovascular Conditions:

1. Coronary Atherosclerosis Homocysteine is a test specific for atheroesclerosisAtherosclerosis is the abnormal accumulation of lipid deposits and fibrous tissue within arterial walls and lumen.In coronary atherosclerosis, blockages and narrowing of the coronary vessels reduce blood flow to the myocardium.Cardiovascular disease is the leading cause of death in the United States for men and women of all racial and ethnic groups.CAD, coronary artery disease, is the most prevalent cardiovascular disease in adults.

Pathophysiology of Atherosclerosis Inflammation (red and swollen area)Coagulation (stop bleeding)Bradikinin, which causes the pain

-Anywhere there is a ischemia the goal is to reperfuse

Risk Factors

Non-ModifiableFamily Hx of CADOlder than 45 years oldGender (men earlier than women)Race

ModifiableHyperlipidemiaSmokingHTNDMObesityPhysical inactivityLaboratory TestsLipid profile: to determine risk of developing atheroclerosisTotal serum lipids= 400-800 mg/dLTriglycerides: lipids stored in fat tissue; normal 100-200 mg/dLCholesterol: main lipid associated with CAD; normal < 200mg/dLLipoproteins: proteins in the blood to transport cholesterol, triglycerides and other fatsHDL= 35-70 mg/dL (M); 35-85 mg/dL (F)LDL= < 160 mg/dLMedicationsHMG-COA Reductase InhibitorsStatins- Atorvastatin ( Lipitor)Nicotinic AcidsNiacins (flushing, like a tomato)Fibric AcidsGemfibrozil ( Lopid)Bile Acid SequestrantsCholestyramine ( Questran)Cholesterol Absorption InhibitorsEzetimibe (Zetia)Omega-3-acidFish oilsThe main goal of all this categories is to lower cholesterolThe main side effect of this meds is - Myalgia (muscle pain) - GI bloating, constipation, dispepcia (GERD)- Myositis (inflammation of muscle)

Clinical ManifestationsSymptoms are due to myocardial ischemiaSymptoms and complications are related to the location and degree of vessel obstructionAngina pectoris (Ischemia)Myocardial infarction (if the ischemia wasnt corrected then MI happens)Heart failureSudden cardiac death (heart suddenly stops beating)

Clinical ManifestationsThe most common symptom of myocardial ischemia is chest pain; however, some individuals may be asymptomatic or have atypical symptoms such as weakness, dyspnea, and nausea.Atypical symptoms are more common in women and in persons who are older, or who have a history of heart failure or diabetes. (nausea, weight gain)

2. Angina PectorisCAD (the buildup of plaque in the arteries lead to angina pectoris) A syndrome characterized by episodes or paroxysmal pain or pressure in the anterior chest caused by insufficient coronary blood flow. Physical exertion or emotional stress increases myocardial oxygen demand and the coronary vessels are unable to supply sufficient blood flow to meet the oxygen demand.

- 3 types of Anginaa) Stable angina: exertionalWith stable angina, the pt take the nitro, and pain goes away.

b) Unstable angina:(preinfarction) exertional- with exercise or stressThis one happens right before the MIIt is not relieve with med and rest. Need to go to ER INMEDIATELY

c) Variant angina: (prinzmetals) spasms of coronary arterySpasm means smaller (small blood vessel)

With angina the main med is nytroglicerin (1 SL) and if after 5 min still hurts, go to ERCOSTOCHONDRIATIS (MUSCLE PAIN) is often confused with chest pain(GERD, PNEUMONIA, PANIC ATTACKS) can be confused with heart attack

For Angina the main thing is reperfuse !!!

Angina pain varies from mild to severeMay be described as tightness, choking, or a heavy sensation.Frequently retrosternal and may radiate to neck, jaw, shoulders, back or arms (usually left).Anxiety frequently accompanies the pain.Other symptoms may occur: dyspnea/shortness of breath, dizziness, nausea, and vomiting.The pain of typical angina subsides with rest or NTG.Unstable angina is characterized by increased frequency and severity and is not relieved by rest and NTG. Requires medical intervention!

TreatmentTreatment seeks to decrease myocardial oxygen demand and increase oxygen supplyMedicationsOxygenReduce and control risk factorsReperfusion therapy may also be done

MedicationsNitroglycerinBeta-adrenergic blocking agents (to decrease the heart and the demand of O2)Calcium channel blocking agents (to decrease the heart and the demand of O2)Antiplatelet and anticoagulant medicationsAspirinClopidogrel and ticlopidine (Plavix)HeparinGlycoprotein IIB/IIIa agents

Treatment of Angina PainTreatment of angina pain is a priority nursing concern.Patient is to stop all activity and sit or rest in bed.Assess the patient while performing other necessary interventions. Assessment includes VS, and observation for respiratory distress, and assessment of pain. In the hospital setting, the ECG is assessed or obtained.Administer oxygen.Administer medications as ordered or by protocol, usually NTG.Collaborative ProblemsAcute pulmonary edemaHeart failureCardiogenic shock (shock is always related to lack of perfusion)Dysrhythmias and cardiac arrestMyocardial infarction

Patient TeachingLifestyle changes and reduction of risk factorsExplore, recognize, and adapt behaviors to avoid to reduce the incidence of episodes of ischemiaTeaching regarding disease processMedicationsStress reduction (bc stress increase SNS)When to seek emergency careAngina Pectoris ReviewWarning sign of impending MIWomen and older adults present atypically3 typesStable angina: exertionalUnstable angina:( preinfarction) exertional- with exercise or stressVariant angina: (prinzmetals) spasms of coronary arteryPain unrelieved by rest or nitro and lasting more than 15 min differentiate angina from MIPrecipitated by exertion or stressRelieved by rest or nitroSymptoms last < 15 minAngina ReviewClient education:Stop activity and restPlace nitro under tongueShould be a bite to the med3 in 15 minutes if not go to ERHEADACHE is most common s/e of nitroEncourage patient to sit and lie down slowlyEncourage smoking cessationDiet and lifestyle modificationGet cholesterol and B/P checked regularlyRemain physically active

Angina- Nursing DiagnosisRisk or decreased cardiac tissue perfusionAnxiety related to cardiac symptoms and possible deathDeficient knowledgeNoncompliance

Myocardial InfarctionAn area of the myocardium is permanently destroyed. Usually caused by reduced blood flow in a coronary artery due to rupture of an atherosclerotic plaque and subsequent occlusion of the artery by a thrombus.In unstable angina, the plaque ruptures but the artery is not completely occluded. Unstable angina and acute myocardial infarction are considered the same process but at different point on the continuum.The term acute coronary syndrome includes unstable angina and myocardial infarction.

MIBlockage of one or more of the coronary arteriesCauses:Arteriosclerosis, emboli, thrombus, shock, hemorrhage, hypoxia leading got necrosisClassic sign: substernal pain or feeling of heaviness on chestPatients may report:Substernal pain or pain over pericardium 15 minPain that is heavy and radiating down left armSpontaneous pain not relived by nitro or restPain that radiates to jawPain accompanied by SOB, pallor, diaphoresis, N/VHR, B/P, temp, RRDiagnosisEKGAngina= ST depression and/or T wave inversion (ischemia)MI= T wave inversion (ischemia), ST elevation (injury), and abnormal Q wave (necrosis)When cardiac muscle suffers ischemic injury, cardiac enzymes are released into the blood stream providing specific markersMyoglobinCK-MBTroponin ITroponin TThallium scans: shows absentCardiac Cath: evaluates blockage

Laboratory Tests Cardiac biomarkers Serum Enzymes: Creatinine Kinase (CK), CK-MB CK formerly known as (CPK)- elevation indicates muscle injury CK-MB: specific to myocardial muscle, rises within 6 hours of injury and peaks at 18 hours post injury and returns to normal within 2-3 days. Useful in DX of MI Lactic dehydrogenase (LDH) Found in many body tissues; elevation is detected within 24-72 hours after MI,peaks in 3-4 days and returns to normal around 2 weeks. Useful for delayed DX of MI Troponin T and I Onset is before CK-MB in MI; peaks at 24 hours and returns to normal around 2 weeks; provides early sensitivity More specific to cardiac injury for DX of MIManagementMonitoringV/S q15 until stableEKG continuous monitoring (within 10 min in ER)Location, severity, quality of painHourly outputLabsMONAWhen B/P falls rapidly= dopamineThrombolytics= streptokinase, retavasePromote energy conservationMedicationsVasodilatorsNitroglycerinAnalgesicsMorphineBeta-blockers/ Calcium Channel BlockersLopressor, Norvasc-CardizemThrombolytic agentsStreptokinaseAntiplateletAspirin, PlavixAnticoagulantsHeparin, LovenoxGlycoprotein inhibitorsIntegrillin (blocks binding of fibrinogen=blocked platelet aggregation)

MISurgical InterventionsPercutaneous transluminal coronary angioplasty (PTCA)Coronary artery bypass graft (CABG)ComplicationsHeart failure and cardiogenic shockIschemic mitral regurgitationVentricular aneurysm/ruptureDysrhythmiasCollaborative ProblemsAcute pulmonary edemaHeart failureCardiogenic shockDysrhythmias and cardiac arrestPericardial effusion and cardiac tamponade

Invasive Coronary Artery ProceduresAKA: Percutaneous Coronary Interventions (PCI)Percutaneous Transluminal Coronary AngioplastyA balloon tipped catheter is used to open blocked coronary vessels and resolve ischemiaPurpose is to improve blood flow within the coronary artery by compressing andcracking the atheromaCatheters are usually introduced into the femoral artery up to the aorta and into the coronary arteriesAngiography is performed using dye to identify the blockageCoronary Artery StentA metal mesh that provides structural support to a vessel at risk of acute closureAtherectomyAn invasive interventional procedure that involves the removal of the atheroma,or plaque from the coronary artery by cutting, shaving or grindingBrachytherapyReduces the recurrence of obstruction, preventing vessel restenosis by inhibitingsmooth muscle cell proliferationComplications of PCI Complications during a PCI procedure Dissection Perforation Abrupt closure Vasospasm of coronary artery Acute MI Acute dysrhythmias Cardiac arrest Complications after PCI procedure Abrupt closure Bleeding at insertion site Retroperitoneal bleeding Hematoma Arterial occlusion Acute renal failure Coronary Artery Bypass Graft (CABG) a blood vessel is grafted to an occluded coronary artery so that blood can flow beyond the occlusion Indications for CABG Alleviation of angina that cannot be controlled with medication or PCI Treatment of left main coronary artery stenosis or multivessel CAD Prevention and treatment of MI, dysrhythmias or heart failure Complications of CABG Hemorrhage Dysrhythmias MINursing Management-CABGPre-operativeAssessing the patientReducing the fear and anxietyMonitoring and managing potential complicationsProviding patient teachingPostoperativeAssessing the patientMonitoring for complicationsRestoring cardiac outputPromoting adequate gas exchangeMaintaining fluid and electrolyte balanceRelieving painMaintaining adequate tissue perfusionMaintaining normal body temperature

Potential Complications of Cardiac SXHypovolemiaPersistent bleedingCardiac tamponadeFluid overloadHTNTachydysrhythmiasBradycardiaCardiac failureMIHypothermia