CARDIAC DISORDERS Anatomy and Physiology Cardiac Muscle Contract as a single unit Simultaneous contraction due to depolarizing at the

he same time Intercalated disk to speed depolarization Automaticity

Action Potential

Cardiac Conduction Sinoatrial (SA) node Fires at 60100 beats/minute Intranodal pathway Atrioventricular (AV) node Fires at 40-60 beats/minute Atrioventricular bundle of His Ventricular tissue fires at 20-40 beats/minute and can occur at this point and down Right and left bundle branches Purkinje fibers

The force or pressure at which the blood is ejected from the ventricle Equated with systemic vascular resistance (SVR) Contractility Coronary Artery

Cardiac Output/Index Cardiac output CO = HR (beats/minute) X SV (liters/beat) Normal adult: 4-8 liters/minute Cardiac index CI = CO(liter/minute)/Body surface area (m2) Normal adult: 2.8-4.2 liter/minute/m2 Normalizes liter flow to body size Arterial and Venous Pressure Relationship

Physical Exam Inspection General appearance Jugular venous distension (JVD) Skin Extremities Palpation Pulses Point of maximal impulse (PMI) Percussion Auscultation Good stethoscope Positioning Normal tones S1/S2 Extra tones S3/S4 Murmurs Rubs Jugular Vein Site

Stroke Volume The amount of blood ejected by the left ventricle Preload The amount of stretch placed on the cardiac muscle just prior to systole Afterload

Grade 3 Moderately loud Grade 4 Loud with a thrill Grade 5 Very loud with an easily palpable thrill Grade 6 Very loud, no stethoscope needed, palpable and visible thrill

Jugular Vein Distention Assessment

Stethoscope Placement

Murmurs Timing Location Transmission Pitch Quality Intensity Grade 1 Barely audible Grade 2 Clearly audible

Congestive Hearth Failure Heart Failure a condition in which the heart's function as a pump to deliver oxygen rich blood to the body is inadequate to meet the body's needs. caused by 1) diseases that weaken the heart muscle 2) diseases that cause stiffening of the heart muscles 3) diseases that increase oxygen demand by the body tissue beyond the capability of the heart to deliver Acute versus chronic Acute: sudden onset of symptoms over hours or days Chronic: limitations on a daily basis Left- versus right-sided heart failure Left-sided: failure of the left ventricle to fill or empty Can be systolic or diastolic in nature Right-sided failure: due to pulmonary disease or pulmonary hypertension Classification of Heart Failure Class I No limitation Class II Slight limitation of physical activity Class III Marked limitation of physical activity with some symptoms at rest Class IV Unable to participate in physical activity, symptoms occur at rest (cardiac cripple)

Statistics A coronary event happens every 26 sec in the USA The death rate for coronary heart disease African American men 262/100,000 White men 228.4/100,000 African American women 176.7/100,000 White women 137.4/100,000 Etiology coronary artery disease high blood pressure(hypertension) longstanding alcohol abuse disorders of the heart valves. Less common causes include viral infections of the stiffening of the heart muscle thyroid disorders disorders of the heart rhythm NSAID, Steroid, Diabetic Meds, & Ca channel blocker Pathophysiology- LSCHF Left Side Heart Failure Dyspnea Paroxysmal Nocturial Dysnea (PND) Orthopnea Rales/Crackles Blood Tinged Frothy Sputum Wheezing (Cardiac Asthma) Moist Cough Dizziness Syncope Fatigue Weakness Anorexia Hypokalemia Clubbing of Fingers Pulsus Alterans

Pathophysiology-RSCHF Neck Vein Engorgement Hepatomegaly Portal Hypertension Ascites Peripheral Edema (Pitting/Dependent) Spleenomegaly Jaundice Internal Hemorrhoids

Leg Varicosities Weight Gain Elevated CVP Reading Nocturia Diagnostic Examination Electrocardiogram (EKG) Echocardiogram Chest radiograph Stress Test Tracer Studies / Radio Active Imaging Laboratory Examination Complete Blood Count Interleukin-6 and C reactive protein Urinalysis TNF-alpha Treatment Life style change Medication Ace Inhibitor Beta Blocker Digoxin Diuretics ( furosemide and Spironolactone) Hearth transplant Ventricular assistive device Myocardial Infarction Angina Pectoris Stable chronic stable angina, classic angina Paroxysmal, occurs with physical exertion Relieved by rest or nitroglycerin Unstable preinfarction angina or crescendo angina More prolonged and severe Need to be treated immediately Variant Prinzmetals angina, vasospastic angina Result of coronary artery spasm Occurs at rest Myocardial Infarction Inflammation Plaque rupture Thrombus formation Irreversible damage starts in 20 to 40 minutes. This process will continue for several hours Risk Factors Uncontrollable Age Heredity Race Sex Modifiable Cigarette smoking High cholesterol

Hypertension Physical inactivity Obesity Diabetes mellitus

Pathophysiology Location of the Infarction Anterior Inferior Posterior Lateral Septal Type of Infarction Q-wave Infarcted the full muscle wall Formation of pathological Q waves in area of infarct Greater then one small box in duration Deeper then 1/3 of the R wave NonQ-wave Infarcted only partial amount of muscle wall ECG Changes

Radiating Anginal Pain

Diagnostics Electrocardiogram Echocardiogram

 Coronary Angiography Treatment Life Style change MONA (Morphine, Oxygen, Nitrates, Anticoagulant) Beta Blocker ACE Statin Anticoagulant Therapy Heparin Thrombolytic Therapy Streptokinase Percutaneous Trans CoronaryAngiography Coronary artery Bypass Surgery (CABG) IABP Stenting

Arrhythmia Arrhythmias Disorders of the formation and/or conduction of electrical impulses in the heart Cause disturbances of heart rate and/or heart rhythm May be evidenced by changes in hemodynamics Diagnosed by analyzing electrocardiogram The Electrocardiogram Defines the graphic representation of the electrical activity of the heart The printed record of the electrical activity of the heart is called a rhythm strip or an ECG strip. ECG Interpretation P wave represents atrial depolarization QRS complex represents ventricular depolarization T wave represents ventricular repolarization U wave may represent repolarization of Purkinje fibers. May also be seen in hypokalemia, hypertension, or heart disease Information Obtainable from ECG Rhythm Strip Analysis

Breakdown of an ECG

P-Wave SA node fires, sends the electrical impulse outward to stimulate both atria and manifests as P-wave. Approximately 0.10 seconds in length

QRS Complex Impulse from the Bundle of HIS throughout the ventricular muscles Measures less than 0.12 seconds or less than 3 small squares on the ECG paper

aP

Interpretation of an ECG Strip Step 1: Heart Rate Step 2: Heart Rhythm Step 3: P P-Wave Step 4: PRI Step 5: QRS Complex Heart Rate PR Interval (PRI) Time which impulse travels from the SA node to the atria and downward to the ventricles 6-Second Method: Have a six second strip, count the QRS complexes and multiple by 10.

What is the rate on this rhythm strip?

2. Are QRS intervals less than 0.12 seconds (narrow)? If so, the complex is most likely supraventricular in origin. 3. Are QRS complexes similar in appearance across the ECG strip?

Heart Rhythm Heart rhythm are classified as regular or irregular. Can calculate the heart rhythm involves establishing a pattern of QRS complexes occurrence. Measure ventricular rhythm by measuring the interval between R R-to to-R waves and atrial rhythm by measuring the P P-to toP waves. Interval > than 0.06 seconds, irregular The P Wave 5 questions: 1. Are P P-Waves present? 2. Are P P-Waves occurring regularly? 3. Is there a P P-Wave for each QRS? 4. Are the P P-Waves smooth, rounded, and upright in appearance, or are they inverted? 5. Do all P P-Waves look similar? The PRI Normal length of the PRI is 0.12 to 0.20 second (3 3-5 small squares) 3 Questions to ask: 1. Are PRI greater that 0.20 seconds? 2. Are PRI less than 0.12 seconds? 3. Are the PRIs constant across the ECG strip? The QRS Complex 3 questions to ask: 1. Are QRS intervals greater than 0.12 second (wide)? If so, the complex may be ventricular in orgin

First Rhythm Strip to Identify Step Step Step Step Step 1: 2: 3: 4: 5: Heart RateStep Rate Heart RhythmStep Rhythm PWave PRI Interval QRS ComplexStep Complex

Artifact Four Common Causes: Patient Movement Loose or defective electrodes Improper grounding Faulty ECG apparatus Patient assessment is critical Types of Rhythms Rate: Bradycardia = rate of <60 bpm Normal = rate of 60 60-100 bpm Tachycardia = rate of >100 100160 bpm Where its coming from: Sinus; SA node Atrial Atrial; SA node fails, impulse comes from the; atria ( internodal or the AV node) Ventricular; SA node or AV junction fails, ventricles will shoulder responsibility of pacing the heart Sinus Rhythms Normal Sinus Rhythm (NSR) Sinus Bradycardia Sinus Tachycardia NSR Rhythm

Sinus Bradycardia Rhythm

Atrial Fibrillation

Atrial Rhythms SA node fails to generate an impulse, the atrial tissue or areas in the internodal pathways may initiate an impulse. These are called atrial dysrhythmias Generally not considered life threatening or lethal careful and deliberate patient assessment must be continuous. lifeTypes of Atrial Rhythms Atrial Flutter Atrial Fibrillation Supraventricular Tachycardia Atrial Flutter

Supraventricular Tachycardia

Ventricular Rhythms SA node or the AV junctional tissue fails to initiate an electrical impulse, the ventricles will shoulder the responsibility of pacing the heart. This group of rhythms are called ventricular dysrhythmias An electrical impulse can be instigated from any pacemaker cell in the ventricles, including the bundle branches or the fibers of the Purkinje fibers. Types of Ventricular Rhythms Premature Ventricular Complexes Ventricular Tachycardia Torsades de Pointes Ventricular Fibrillation Asystole Pulseless Electrical Activity (PEA)

Torsades de Pointes French term that signifies the twisting of the points. May wax and wane in amplitude and may flip or twist on its electrical axes. Similar to ventricular tachycardia Caused by hypomagnesemia or by antiarrhythmic drugs

Premature Ventricular Complexes (PVCs)

Ventricular Fibrillation Ventricular Tachycardia

Second Second-Degree AV Block (Mobitz Type II) Third Degree AV Block (Complete)

First Degree AV Block

Asystole

Second Degree AV Block (Mobitz Type I) or Wenckebach Second-

Pulseless Electrical Activity (PEA) The absence of a palpable pulse and myocardial muscle activity with the presence of organized electrical activity (excluding VT and VF) on cardiac monitor. It is not an actual rhythm, it represents a clinical condition wherein the patient is clinically dead, despite the fact that some type of organized rhythm appears on the monitor Types of Heart Blocks First Degree AV Block Second Second-Degree AV Block (Mobitz Type I) or Wenckebach

Second-Degree AV Block (Mobitz Type I) or Wenckebach

SecondSeconDegree AV Block d-(Mobitz Type II)

Limb Lead Deflection

Third Degree AV Block (Complete)

Pacemaker Therapy Provides electrical stimuli to heart muscle Used for slower-than-normal impulse formation, to control some tachycardias, or for advanced heart failure May be permanent or temporary NASPE-BPEG code First letter identifies chambers being paced Second letter describes the chambers being sensed Third letter describes type of response by pacemaker to what is sensed

Artificial Pacemaker

Antilipemic agents Vasoconstrictors Anticoagulants Platelet inhibitors Thrombolytic agents Colony stimulating factors

Three Ways Drugs Can Affect Heart Action Inotropic = increase/decrease force of myocardial contraction. Chronotropic= increase/decrease heart rate. Dromotropic= increase/decrease conduction of electrical impulses Cardiac Medication Cardiac Glycosides Strengthen the heartbeat Congestive heart failure Digoxin (Lanoxin)-(0.25mg or 0.125mg). Digitalization Monitoring apical pulse Digitalis levels: 0.5-2.0 Digitalis Toxic side effects Treatment of digitalis toxicity Contraindications or extreme caution Interactions Patient education Anti-arrhythmic Agents Suppress various types of arrhythmias Need for accurate and timely reporting of vital signs and observations Alert for signs of hypotension and bradycardia Anti-arrhythmic Agents Adrenergic blockers Calcium channel blockers Disopyramide Lidocaine Tonocard (tocainide) Procainamide Quinidine Patient education Antihypertensives Lower blood pressure Prescribed on trial basis Monitor VS and observe for side effects Common side effects is hypotension

Cardioversion and Defibrillation Delivery of electrical current to depolarize a critical mass of myocardial cells When cells repolarize the SA node, is usually able to recapture its role as pacemaker of heart Cardioversion involves use of timed electrical current to terminate a tachydysrhythmia Defibrillation is used in emergency situations as treatment for ventricular fibrillation and pulseless VT

PHARMACOLOGY Cardiovascular Drugs Medications that affect heart and blood vessels May also alter blood component Categories Cardiac glycosides Antiarrhythmic agents Antihypertensives Vasodilators

 Postural hypotension Anti Hypertensive Drugs Diuretics Beta Adrenergic Blocker Hypertension with angina, postmyocardial infarction, and certain arrhythmias Angiotensin Converting Enzyme (ACE) Inhibitor Decrease vasoconstriction Angiotensin Receptor Blocker Similar to ACE inhibitors as they block vasoconstriction, but at different sites Coronary Vasodilators Treat angina by dilating blood vessels Ischemia Angina pectoris Obstruction or constriction of coronary arteries Coronary Dilator Nitroglycerin Isosorbide (Isordil, Sorbitrate) Side effects Contraindications or extreme caution Interactions Patient education Anti Lipemic Agents Antilipemic Agents Statins Lipitor=atorvastatin Lescol=fluvastatin Mevacor-altocor=lovastatin Pravachol=pravastatin Crestor=rosuvastatin Zocor= simvastatin Vasoconstrictors Dopamine Dobutamine Epinephrine Norepinephrine Anti Coagulants Heparin Standard Heparin Low Molecular weight heparin Coumarine Derivatives Coumadin Platelet Inhibitor Therapy Decrease platelet clumping

Dipyridamole (Persantine) Aspirin Clopidogrel (Plavix)

Thrombolytic Dissolve clots (fibrinolysis) after they have formed IV in less than 6 hours after MI or CVA Bleeding Most serious complication Streptokinase LABORATORY AND DIAGNOSTIC Cardio Biomarkers CK CKMB Myoglobulin Troponin LDH AST CRP BNP Cardio Diagnostic Exam Angiography Cardiac Catheterization Computed Tomography (CT scan) Echocardiography Intravascular Ultrasound (IVUS)/Intravascular Echocardiography Stress Echocardiography Transesophageal Echocardiography (TEE) Electrocardiogram (ECG or EKG) Electrophysiology Studies (EPS) Exercise Stress Test Holter Monitoring Magnetic Resonance Angiography (MRA) Cardiac Magnetic Resonance Imaging (Cardiac MRI) Nuclear (Thallium) Stress Test Positron Emission Tomography (PET scan) Cardiac Catheterization Unit

NURSING CONSIDERATION RECORD weight DAILY: - early morning, post micturition, pre food1. Weight on Admission _________KG Report fluctuations in weight (Rapid weight - Gain/Loss) to Medical Assess level of edema daily and check pressure areas NURSING ACTION: Fluid balance will be recorded and documented each 24-hour period Restrict Fluid to 1.5 Litres or 2 Litres if patient is fluid over loaded1 Encourage a LOW SODIUM diet Offer patient frequent mouth washes and perform regular mouth care Refer to dietician if appropriate. Administer Oxygen as prescribed drug chart and record oxygen NURSING CONSIDERATION Record Respiratory Rate - Ensure patient is sat in an upright position.

Monitor Blood Pressure (Lying & standing), Pulse according to observation plan report symptomatic hypotension and/or bradycardia (ACE Inhibitors, Diuretics [furosemide,bumetanide,metolazo ne,Spironolactone] BBlockers [Bisoprolol fumerate, Carvedilol]) Watch out for arrhythmia Check if pace maker is pacing Jugular vein distention Hemodynamic Monitoring