Disorders of Cardiac Function NURS 315/501 Kathryn T. Von Rueden RN, MS, FCCM University of Maryland School of Nursing
Global Tissue Oxygenation Made Ridiculously Simple SvO2 = 75% 25% Venous Oxygen Delivery Arterial Oxygen Delivery Oxygen C...
Coronary Circulation
Cardiac Conduction System <ul><li>Conduction system stimulates the myocardium to contract & pump blood </li></ul><ul><li>C...
Anatomy of the Conduction System SA Node AV Node Bundle of His Bundle branches Purkinje fibers Porth, 2007,  Essentials of...
SA Node <ul><li>Pacemaker of the heart </li></ul><ul><li>Impulses originate here </li></ul><ul><li>Located in posterior wa...
AV Node <ul><li>Connects the atria & ventricles, provides one way conduction </li></ul><ul><ul><li>Would beat independentl...
Purkinjie Fibers <ul><li>Supplies the ventricles </li></ul><ul><li>Large fibers, rapid conduction for swift & efficient ej...
Action Potentials (AP) <ul><li>Stimulus  </li></ul><ul><li>   excitable tissues (muscle & conduction system)  </li></ul><...
SLOW  SA & AV Nodes FAST   Purkinje Fiber & Muscle
Cardiac Action Potentials <ul><li>3 types of membrane ion channels that contribute to voltage changes during the phases of...
Three Phases of AP <ul><li>Resting </li></ul><ul><ul><li>Membrane is relatively permeable to K + , but much less so to Na ...
Cardiac Muscle Cell Firing <ul><li>Cells begin with a negative charge: resting membrane potential </li></ul><ul><li>Calciu...
Cardiac Muscle Cell Firing (cont.) <ul><li>At threshold potential, more Na +  channels open </li></ul><ul><li>Na +  rushes...
Cardiac Muscle Cell Firing (cont.) <ul><li>K +  channels open </li></ul><ul><li>K +  diffuses out, making the cell negativ...
Cardiac Muscle Cell Firing (cont.) <ul><li>During  plateau , the muscle  contracts strongly </li></ul><ul><li>Then the Ca ...
Cardiac Action Potentials <ul><li>Unlike nerve cells, cardiac cells have five phases in their action potential </li></ul><...
Cardiac Muscle Action Potential 5 Phases Phase 0 :  Upstroke, rapid depolarization Phase 1:   Early, short repolarization ...
Cardiac Muscle Cell Contraction <ul><li>During Phase 2, the plateau, calcium ion enters the muscle cell, causing it to con...
Lehne 5 th  ed  Figure 47-2 Myocardium & His-Purkinje System SA Node & AV Node <ul><li>Why are action potentials important...
Cardiac Conduction  &  Rhythm Disorders
ECG: Relationship  to Action Potential <ul><li>Electrical events recorded on ECG </li></ul><ul><li>Electrical events prece...
Lehne 5 th  ed Figure 47-3 Electrical event precedes mechanical event !!!
Porth 2007, Figure 16-12 P wave PR Interval QRS complex T wave:  Repolarization
Disorders of Cardiac Rhythm  and Conduction  : 2 Types <ul><li>Dysrhythmias (or arrhythmias) </li></ul><ul><ul><li>Term us...
Disorders of Cardiac Rhythm  and Conduction <ul><li>2 types of disorders of the cardiac conduction system </li></ul><ul><u...
Causes <ul><li>Congenital defects in conduction system </li></ul><ul><li>Degenerative changes </li></ul><ul><li>Ischemia a...
Sinus Node Rhythms <ul><li>Normal Sinus Rhythm </li></ul><ul><ul><li>P wave precedes each QRS, RR intervals reg, rate 60-1...
Lehne 5 th  ed  Figure 47-2 Myocardium & His-Purkinje System SA Node & AV Node Class II Antidysrhythmic
Class II Antidysrhythmic  Beta Blockers <ul><li>Depress Phase 4 in depolarization </li></ul><ul><li>Nonselective:  Carvedi...
Class II Antidysrhythmic  Beta Blockers <ul><li>ECG </li></ul><ul><ul><li>Prolong PR & bradycardia </li></ul></ul><ul><li>...
Beta Blocker: Adverse effects <ul><li>Hypotension </li></ul><ul><li>Syncope </li></ul><ul><li>Precipitate HF </li></ul><ul...
Beta Blocker Administration  (remember from last week) Drug Route ½ Life (hrs) Indication Esmolol IV ONLY! 0.15 Dysrh, ang...
Atrial Dysrhythmias Atrial Fibrillation :  Chaotic & disorganized current. Atria are depolarizing without contracting (jus...
A-Fib treatment: Digoxin <ul><li>A cardiac glycoside that is used for atrial fibrillation or atrial flutter. </li></ul><ul...
Digoxin <ul><li>Mechanism of Action: </li></ul><ul><li>Inhibits Na + -K +  ATPase; more intracellular calcium available </...
Lehne 6 th  ed Figure 47-4
Digoxin:  Pharmacokinetics Absorption 60 – 80% (tabs) 70 – 85% (elixir) 90 – 100% (caps) Metabolism Liver Half Life 5-7 DA...
Digoxin Administration Considerations <ul><li>PO or IV (mcg NOT mg) </li></ul><ul><ul><li>“ Digitalization” </li></ul></ul...
Adverse effect & S/S digoxin toxicity <ul><ul><li>Digoxin induced dysrhythmias </li></ul></ul><ul><ul><ul><li>All types!  ...
Digoxin Contraindications & Precautions Contraindications Precautions 2 nd /3 rd   degree  heart block V. Fib/V. Tach Sick...
Digoxin Additional Considerations <ul><li>Potassium levels  </li></ul><ul><li>Keep in 3.5 – 5.0 mEq/L range </li></ul><ul>...
Drug  Drug Interactions <ul><li>Reduce digoxin therapeutic effect   </li></ul><ul><li>ACE-I & ARBs </li></ul><ul><ul><li>...
Drug  Drug Interactions Increase risk of digoxin toxicity <ul><li>Calcium channel blockers (verapamil) </li></ul><ul><ul>...
Digoxin:  Nursing Implications Apical pulse for 1 min. & document Monitor ECG Monitor potassium & dig levels
A-Fib, PSVT Treatment Class IV Antidysrhythmic  Calcium Channel Blockers <ul><li>Verapamil, diltazem </li></ul><ul><li>Mec...
Lehne 5 th  ed  Figure 47-2 Myocardium & His-Purkinje System SA Node & AV Node
Class IV Antidysrhythmic  Calcium Channel Blockers (verapamil, diltiazem) <ul><li>3 effects on heart </li></ul><ul><li>Slo...
Verapamil & Diltiazem Adverse Effects ( Remember from last week) <ul><li>Cardiac: </li></ul><ul><li>Bradycardia </li></ul>...
Disorders of Atrioventricular Conduction 1st degree AV block:  Slightly prolonged PR interval;  ALL  atrial impulses are c...
Case study: Digoxin toxicity Serum dig level = 1.7 ng.ml  (0.5-1.1 desired) 3 rd  degree AV Block Temporary pacemaker inse...
Complete A-V block with 100% atrio-ventricular pacing Atrial  Pacing spike Ventricular  Pacing spike P  QRS
Ventricular Dysrhythmias: More Serious! PVC:   Ventricles contract prematurely.  W/ a PVC, diastolic volume is insufficien...
Lehne 5 th  ed  Figure 47-2 Myocardium & His-Purkinje System SA Node & AV Node Class I Antidysrhythmic
Class 1B: Lidocaine  Ventricular Dysrhthmias
Class 1B: Lidocaine <ul><li>Effect on Heart & ECG </li></ul><ul><ul><li>Blocks Na+ channels   slow conduction thru atria,...
Lidocaine: Precautions & Adverse Effects <ul><li>Metabolized by Liver </li></ul><ul><li>Therapeutic range 1.5 – 5.0 microg...
Lidocaine: Administration <ul><li>IV Push </li></ul><ul><ul><li>50-100mg (1mg/kg) </li></ul></ul><ul><li>Infusion </li></u...
Class III Antidysrhythmic <ul><li>Potassium Channel Blockers:   Amiodarone </li></ul><ul><li>Approved  for VT & VF  </li><...
Lehne 5 th  ed  Figure 47-2 Myocardium & His-Purkinje System SA Node & AV Node Class III Antidysrhythmic
Non-Pharmacologic  Treatment of  Dysrhythmias <ul><li>Cardioversion </li></ul><ul><ul><li>Atrial fib </li></ul></ul><ul><u...
Automated External Defibrillator <ul><li>Cardiac Arrest, AED “interrogates” rhythm. </li></ul><ul><li>Tells user what to d...
Non-Pharmacologic  Treatment of  Dysrhythmias <ul><li>Implantable Cardioverter/Defibrillator </li></ul><ul><ul><li>Like a ...
Antidysrhythmic Drugs: Summary <ul><li>Class I   </li></ul><ul><ul><li>Depress phase 0 in depolarization </li></ul></ul><u...
<ul><li>Class III </li></ul><ul><ul><li>Prolong phase 3 (repolarization) </li></ul></ul><ul><li>Class IV </li></ul><ul><ul...
Management of  Cardiac Dysrhythmias REMEMBER: Many drugs used to treat dysrhythmias also may worsen them  or cause new ones!
Coronary Heart Disease  &  Acute Myocardial Infarction (MI or AMI)
Coronary Circulation <ul><li>Two main coronary arteries arise from coronary sinus (above aortic valve) </li></ul><ul><li>P...
Coronary Circulation LV LV
Ischemic Heart Disease a.k.a Coronary Heart Disease  a.k.a Coronary Artery Disease Angina Myocardial Infarction
Coronary Heart Disease <ul><li>Heart disease caused by impaired coronary blood flow (atherosclerosis) </li></ul><ul><li>Ca...
Assessment of Coronary  Blood Flow <ul><li>ECG </li></ul><ul><li>Exercise Stress Testing </li></ul><ul><li>Pharmacologic S...
Collateral Circulation <ul><li>With gradual occlusion of large coronary vessels, the smaller collateral vessels    in siz...
Collateral Circulation
Pathogenesis of CAD: Atherosclerosis <ul><li>Most common cause of CAD </li></ul><ul><li>Plaque disruption is most frequent...
Plaque <ul><li>Plaques typically do not occlude the whole coronary artery but produce a narrowing that restricts blood flo...
Atherosclerosis in Coronary Artery <ul><li>Plaque rupture & disruption of atheroma    </li></ul><ul><li>   lipid core/co...
Review of Terms Related to CHD <ul><li>Angina:  symptomatic paroxysmal chest pain or pressure sensation associated with tr...
Plaque Rupture <ul><li>Spontaneous </li></ul><ul><ul><li>SNS activation   BP,    HR,    contraction </li></ul></ul><ul>...
“ Severe” coronary stenosis and vulnerable plaques co-exist Califf, Atlas of Heart Diseases 2001
Ischemia, Injury, & Infarction  <ul><li>3 Zones of Damage </li></ul><ul><li>Infarction = Necrosis </li></ul><ul><li>-MI, d...
Zones of Tissue Damage <ul><li>Goal is to limit the area of necrosis (infarction) ! </li></ul><ul><li>Necrotic myocardial ...
An Acute MI (AMI) Leaves Behind an  Area of Yellow Necrosis
Pathologic Changes <ul><li>Ischemic areas cease to function within minutes </li></ul><ul><li>Irreversible damage/death to ...
Pathologic Changes  <ul><li>Extent of infarct depends on : </li></ul><ul><li>location </li></ul><ul><li>extent of occlusio...
Pathologic  Changes <ul><li>Transmural infarct </li></ul><ul><ul><li>Full thickness of ventricular wall,  </li></ul></ul><...
Chest Pain Assessment <ul><li>P - Provocation </li></ul><ul><li>Q - Quality </li></ul><ul><li>R – Region/Radiation </li></...
Categories (PQRST) <ul><li>Angina that occurs with stress (physical/emotional) </li></ul><ul><ul><li>Relieved within minut...
Stable Angina <ul><li>Fixed coronary obstruction </li></ul><ul><li> 0 2  Demand       0 2  supply   pain </li></ul><ul...
Angina Typically precordial, substernal Usual distribution of pain Less common sites of pain distribution
Variant or Vasospastic Angina <ul><li>“ Prinzmetal’s angina” </li></ul><ul><li>Due to coronary artery spasms  </li></ul><u...
Hamon M and Hamon M. N Engl J Med 2006;355:2236 A 38-year-old man was scheduled to undergo invasive coronary angiography a...
Acute Coronary Syndrome (ACS) NSTEMI STEMI Unstable or ruptured plaque
Acute Coronary Syndrome (ACS)
Unstable Angina <ul><li>Clinical syndrome of myocardial ischemia ranging between stable angina and MI </li></ul><ul><li>Us...
Porth, 2007,  Essentials of Pathophysiology,  2nd ed., Lippincott, p. 392 .
Acute Coronary Syndrome (ACS)
ST Segment Elevation <ul><li>ST segment elevations are indicative of myocardial damage or ischemia. </li></ul><ul><li>It m...
ECG : STEMI vs NSTEMI
Non ST Segment Elevation Myocardial Infarction   (NSTEMI) How is this different from unstable angina or STEMI? Unstable an...
Porth, 2007,  Essentials of Pathophysiology,  2nd ed., Lippincott, p. 392 .
ST Segment Elevation MI <ul><li>Characterized by ischemia of cardiac tissue </li></ul><ul><li>Area of infarction is determ...
Porth, 2007,  Essentials of Pathophysiology,  2nd ed., Lippincott, p. 392 .
Diagnosis CHD and MI <ul><li>Good history & identification of risk factors </li></ul><ul><li>R/O Other causes of CP, eg GE...
“ Classic” Manifestations of MI <ul><li>Abrupt onset or progression of unstable, non-ST elevation </li></ul><ul><li>Pain i...
ECG Changes <ul><li>T wave inversion </li></ul><ul><li>ST segment elevation </li></ul><ul><li>Abnormal Q wave   </li></ul>...
ST Segments <ul><li>1 st   to change during ischemia or MI because myocardial repolarization is altered. </li></ul><ul><li...
Abnormal Q Waves <ul><li>Develop because there is no depolarizing current conduction from necrotic tissue </li></ul><ul><l...
Serum Markers for Ischemia & MI <ul><li>Necrotic cells release intracellular enzymes into blood stream </li></ul><ul><li>M...
CK-MB <ul><li>CK normal in all muscle cells, has 3 isoenzymes BB, MM, MB </li></ul><ul><li>CK-MB Creatine kinase -myocardi...
Troponin  (TnC, TnI, TnT) <ul><li>Part of the actin-myosin filament </li></ul><ul><li>Rises within 3 hours after MI </li><...
C-Reactive Protein  (CRP) <ul><li>Marker of chronic inflammation </li></ul><ul><li>Maybe a marker of risk </li></ul><ul><l...
Cardiac Markers Hr 1 2 3 4 5 6 7 8 9 10 11 12  Day 2  3  4  5 Troponin CK-MB
NSTEMI Unstable angina No ECG   s Elevation of serum markers Unstable Angina Pain is severe No ECG   s No change in mark...
ACS Case Presentation 1 <ul><li>68 yr male; 3 mos. h/o progressive chest pain; day of adm, with minimal exertion </li></ul...
Management of  Angina & CHD/AMI <ul><li>Goals:  </li></ul><ul><li>Prevent or minimize infarction </li></ul><ul><li>Increas...
Management of  Angina & CHD/AMI <ul><li>Treatment </li></ul><ul><ul><li>Non-pharmacologic: Percutaneous Coronary Intervent...
Acute Management: Reperfusion <ul><li>PTCA/PCI </li></ul><ul><ul><li>ASAP </li></ul></ul><ul><ul><li>With or without throm...
Reperfusion McCance 5 th  Ed, 2006 Figure 30-2
Reperfusion – Balloon Angioplasty, Possibly with Stenting Copyright © 2005 Nucleus Communications, Inc. All rights reserve...
Complication of PCI N Engl J Med 2011;364:453-64.
Administration of Thrombolytic Therapy Must be Done Promptly Giugliano & Braunwald,  Circulation  2003;108;2828-2830 IRA =...
PCI (angioplasty ± stenting) must be done promptly Nallamothu B et al. N Engl J Med 2007;357:1631-1638
Emergency Pain Relief <ul><li>Morphine Sulfate </li></ul><ul><li>Venodilation </li></ul><ul><ul><li>Reduces preload & card...
<ul><li>Nitroglycerin </li></ul><ul><ul><li>Angina </li></ul></ul><ul><ul><li>Acute myocardial infarction </li></ul></ul><...
Nitroglycerin Lehne, 2006 Tables 50-3 and 50-4 Purpose/Onset Administration Duration SL Acute angina 1 – 3 min 0.3 – 0.6 m...
Nitroglycerin Pharmacokinetics <ul><li>Metabolized in the liver </li></ul><ul><li>Excreted by liver & kidneys </li></ul><u...
Nitroglycerin Contraindications <ul><li>Severe hypotension </li></ul><ul><li>Increased ICP </li></ul><ul><li>Cerebral hemo...
Nitroglycerin  Drug  Drug Interactions <ul><li>Alcohol </li></ul><ul><ul><li>SEVERE hypotension; CV collapse </li></ul></...
Chronic HD & Angina Management <ul><li>Nitrates </li></ul><ul><li>Beta Blockers </li></ul><ul><li>Calcium channel blockers...
Nitrates: Chronic Angina Lehne, 2006 Tables 50-3 and 50-4 Purpose/Onset Administration Duration Oral Isosorbide dinitrate ...
Nitroglycerin  Patient/Family Education <ul><li>SL </li></ul><ul><ul><li>Tabs between cheek/lip & gum </li></ul></ul><ul><...
Angina Prophylaxis <ul><li>“ Medical management” of symptomatic coronary artery disease (stable angina) has been shown to ...
Beta-adrenergic Blocking Agents <ul><li>Manage stable angina (not vasospastic) </li></ul><ul><li>Block beta-1 receptors </...
Calcium Channel Blockers <ul><li>Verapamil, diltiazem, nifedipine </li></ul><ul><li>Manage stable & vasospastic angina </l...
<ul><li>Anti-platelet drugs </li></ul><ul><li>Aspirin,  </li></ul><ul><li>clopidorel (Plavix),  </li></ul><ul><li>IIb,IIIa...
Kumar (2003) IIb-IIIa Inhibitors   Abciximab (RePro @ ) Alter Platelet Aggregation <ul><li>-  Onset 2 hours </li></ul><ul>...
Anti-platelet & Anticoagulant Drugs <ul><li>Contraindications  </li></ul><ul><li>Active bleeding </li></ul><ul><li>CVA w/i...
You having an MI ??
Which of the following is present in stable angina? <ul><li>An unstable plaque. </li></ul><ul><li>A ruptured plaque </li><...
Which of the following is  diagnostic  of an acute myocardial infarction? <ul><li>ST segment elevation </li></ul><ul><li>I...
Management of unstable angina or acute myocardial infarction must include interventions/medications that: <ul><li>Increase...
Need a break?
Heart Failure
Heart Failure <ul><li>Failure of the heart to function as a pump </li></ul><ul><li>Normally pumping ability adjusts to bod...
Heart Failure <ul><li>HF involves interplay between 2 factors: </li></ul><ul><ul><li>Inability of failing heart to maintai...
Cardiac Output   Stroke Volume Heart Rate Preload   LVEDV Afterload   SVR Contractility   LVSWI  Determinant of Cardiac Ou...
SV Contractility CO O 2  to  Organs Trigger  Compensatory  Mechanisms Blood volume Vascular resistance Cardiac  work HF
Vicious Cycle of Heart Failure Lehne, 2009,  Pharmacology for Nursing Care, 7th ed., Elsevier, p. 518
Compensatory Mechanisms Maintain Vital Organ Perfusion <ul><li>Compensated heart failure </li></ul><ul><ul><li>Short term ...
Compensatory Mechanisms <ul><li>Frank Starling mechanism </li></ul><ul><li>Increased SNS activity </li></ul><ul><ul><li> ...
Causes of CHF Impaired Cardiac Function Excess Work Demands Myocardial Disease Increased Pressure <ul><li>Cardiomyopathy <...
Heart Failure <ul><li>Pulmonary and/or systemic venous congestion </li></ul><ul><li>Described as </li></ul><ul><ul><li>Sys...
Systolic vs Diastolic Failure <ul><li>Systolic dysfunction </li></ul><ul><ul><li>Impaired ejection  of blood from heart du...
Systolic Dysfunction Impaired ejection    cardiac contractility      CO Conditions that    contractility: ischemic hea...
Diastolic Dysfunction Porth 2005 28-4 Impaired filling    LV Filling       CO Conditions that cause diastolic dysfuncti...
Right-sided vs Left-sided Failure Classified according to side of heart that is affected
“ Backward” “ Forward”
Right Heart Failure (RHF)    fluid  accumulation in systemic venous system    venous congestion     peripheral edema Ca...
Left Heart Failure (LHF) Pathophysiology :    CO     LA & LV EDV & pulmonary pressure     eventually pulmonary edema. ...
BNP: B-Type natriuretic peptide <ul><li>Synthesized in myocardium of ventricles </li></ul><ul><li>Released in response to ...
BNP in  Heart Failure <ul><li>Diagnosis </li></ul><ul><ul><li>BNP < 100, used to rule out new HF  </li></ul></ul><ul><ul><...
HF Classifications ACC/AHA NYHA Functional Class A   High Risk; no structural  disease or symptoms B  Structural disease; ...
Heart Failure Management <ul><li>GOALS </li></ul><ul><li>1. Reduce myocardial restructuring / remodeling </li></ul><ul><ul...
Diuretics Preload Vasodilators Afterload
Diuretic Therapy <ul><li>Furosemide (Lasix) </li></ul><ul><li>Ascending loop of Henle </li></ul><ul><li>Block Na+ & Cl- re...
Loop Diuretics Adverse Effects <ul><li>Hypotension </li></ul><ul><ul><li>Volume loss </li></ul></ul><ul><ul><li>Venodilati...
Afterload Reduction in HF  Vasodilation   -  Decrease resistance to ventricular    ejection of blood -  Improves forward ...
Angiotensin Converting Enzyme Inhibitors (ACE-I) <ul><li>(captopril, lisinopril, enalipril) </li></ul><ul><li>Mechanism of...
Angiotensin II Receptor Blockers (ARBs) <ul><li>(valsartan) </li></ul><ul><li>Mechanism of Action </li></ul><ul><li>Blocks...
ALL  Heart Failure Patients SHOULD BE ON an ACE-I or ARB !!!!!!!! American College of Cardiologists,  TJC, NQF, AHRQ
Beta blockers and HF <ul><li>Selective use due to negative inotropic effect </li></ul><ul><li>Decrease contractility and a...
Digoxin: Considerations in HF <ul><li>Increases intracellular calcium concentration    improves contractility  PLUS  slow...
<ul><li>Aldosterone receptor blocker   (spironolactone [Aldactone]) </li></ul><ul><ul><li>Advanced HF, symptomatic despite...
The renin-angiotensin-aldosterone system contributes to worsening of heart failure and myocardial remodeling. Appropriate ...
A patient has severe mitral stenosis which greatly limits blood flow between the left atrium and the left ventricle.  This...
A patient is newly diagnosed with heart failure.  Which of the following drugs should  always  be prescribed? <ul><li>A be...
Need a break?? Can’t make it any longer….
Disorders of Heart Valves
Valvular Heart Disease <ul><li>Function of the valves is to ensure  unidirectional  flow of blood in the heart </li></ul><...
Stenosis <ul><li>Valve does not open properly </li></ul><ul><li>   resistance to blood flow thru valve </li></ul><ul><li>...
Regurgitation <ul><li>Valve does not close properly </li></ul><ul><li>Permits backflow to occur when valve should be close...
Mitral Valve Prolapse <ul><li>2-7% of the population </li></ul><ul><li>Most asymptomatic </li></ul><ul><li>Usually unknown...
Valvular Heart Disease <ul><li>Valve defects are characterized by heart murmurs resulting from turbulent flow thru valve <...
Diagram in Handout- Use it to figure out murmurs & Problems with blood flow d/t valvular defects!
Mitral Stenosis <ul><li>Incomplete opening of MV during diastole  </li></ul><ul><ul><li>   LA distention  </li></ul></ul>...
Mitral Stenosis: Signs & Symptoms When would you hear a murmur?  DIASTOLE
Mitral Valve Regurgitation <ul><li>Incomplete closure of MV </li></ul><ul><li>During systole, part of LV SV goes forward i...
Mitral Valve Regurgitation <ul><li>Acute </li></ul><ul><ul><li>   forward SV,    regurgitant SV  </li></ul></ul><ul><ul>...
Mitral Valve Regurgitation <ul><li>Management </li></ul><ul><li>Acute  </li></ul><ul><ul><li>Improve forward flow with vas...
Aortic Valve Stenosis <ul><li>   resistance to ejection of blood from LV into aorta </li></ul><ul><li>   resistance    ...
Aortic Valve Regurgitation <ul><li>Incompetent AoV  </li></ul><ul><li>   backflow of blood to LV during diastole  </li></...
Aortic Valve Regurgitation <ul><li>Acute </li></ul><ul><ul><li>Sudden uncompensated    LVEDP    pulmonary edema &    CO...
Valve Disease Summary
Which of the following might produce pulmonary edema? <ul><li>Mitral stenosis </li></ul><ul><li>Pulmonic stenosis </li></u...
Kathryn !!! Pleeeaaase! Release the students! Mmmm…excellent!
Shock: The rude unhinging of the machinery of life!
Shock <ul><li>Adequate perfusion of body tissues depends on: </li></ul><ul><ul><li>Functioning heart to pump 0 2  into sys...
Shock  Impairment of cellular metabolism <ul><li>Impairment of oxygen use </li></ul><ul><ul><li>Aerobic to anaerobic metab...
Global Tissue Oxygenation Made Ridiculously Simple SvO2 = 75% 25% Venous Oxygen Delivery Arterial Oxygen Delivery Oxygen C...
Aerobic Metabolism Anaerobic Metabolism 36 molecules ATP 2 molecules ATP Supports normal  cell function Eventual  cell dys...
4 Types of Circulatory Shock <ul><li>Hypovolemic </li></ul><ul><ul><li>Diminished blood volume    inadequate filling of v...
Compensatory Mechanisms <ul><li>Sympathetic Nervous System </li></ul><ul><li>   Heart rate </li></ul><ul><li>   Respirat...
Cardiogenic Shock
Preload SV Restore Cardiac Pump   Ventricular Contractility Positive Inotropic Agents Depressed Normal Enhanced
Enhance Contractility <ul><li>Beta –1 Effect, increase contractility </li></ul><ul><li>Epinephrine </li></ul><ul><li>Dobut...
Dobutamine <ul><li>Beta-1 selective adrenergic agonist </li></ul><ul><li>First line to increase cardiac output </li></ul><...
Epinephrine <ul><li>Non-selective adrenergic agonist </li></ul><ul><li>First line in cardiac arrest & anaphylaxis </li></u...
Epinephrine <ul><ul><li>Cardiac Arrest </li></ul></ul><ul><ul><li>IV Push  </li></ul></ul><ul><ul><ul><li>Pre-filled syrin...
Cardiogenic Shock Vasodilators Afterload
Afterload Manipulation: Restore perfusion or Decrease Work of Heart <ul><li>   Systemic Vascular  Resistance  (SVR) </li>...
Sodium Nitroprusside (Nipride) <ul><li>Arterial vasodilator   </li></ul><ul><li>reduces resistance to LV ejection </li></u...
Hypovolemic Shock <ul><li>Acute loss of 15-20% of blood volume </li></ul><ul><li>Characterized by    blood volume     in...
Hypovolemic Shock
Clinical Manifestations <ul><li>Mild  </li></ul><ul><ul><li> HR,   BP, cool extremities </li></ul></ul><ul><li>Moderate ...
Frank-Starling Curve: Preload SV LVEDV LV dysfunction Hypovolemia Normal
Restore Intravascular Volume <ul><li>Crystalloid Infusion  Isotonic Fluids </li></ul><ul><li>0.9% NaCl  </li></ul><ul><ul>...
Stop Intravascular Volume Loss  &/or DIC <ul><li>Blood products </li></ul><ul><ul><li>Platelets    plug the holes </li></...
Distributive S hock <ul><ul><li>Loss of vessel tone, enlargement of vascular compartment, displacement of vascular volume ...
Septic Shock <ul><li>Associated with severe infection and the systemic response to the infection. </li></ul><ul><li>Gram n...
Septic shock <ul><li>Endotoxin & inflammatory mediator release   </li></ul><ul><li>Vasodilation    Decrease preload </li...
What is SIRS? Systemic Inflammatory Response Syndrome Often a precursor to sepsis! <ul><li>Clinical response arising from ...
Continuum of S epsis SIRS with a suspected or confirmed infx Sepsis SIRS Septic  Shock ≥ 2 of the following: Temp:  >38°C ...
Sepsis Resuscitation Bundle within 1 st  hour of recognition <ul><li>Obtain serum lactate </li></ul><ul><li>Blood cultures...
Sepsis Resuscitation Bundle within 1 st  6 hours of recognition <ul><li>PRBC for Hgb < 7 g/dl, target 7-9 g/dl </li></ul><...
Catecholamines: Adrenergic Agonists Alpha 1 Beta 1 Beta 2 Dopamine Vasoconstrict Cardiac stimulation Bronchodilate Renal a...
Complications of Shock <ul><li>“ Shock not only stops the machinery, but it wrecks the machinery” (Wiggers) </li></ul><ul>...
Cardiac Output   Stroke Volume Heart Rate Preload   Afterload   Contractility   Management of Shock: Oxygen Delivery SaO2 ...
Global Tissue Oxygenation Made Ridiculously Simple SvO2 = 75% 25% Venous Oxygen Delivery Arterial Oxygen Delivery Oxygen C...
Appropriate treatment of hypotension related to cardiogenic shock includes: <ul><li>Volume infusion </li></ul><ul><li>Vaso...
Appropriate treatment of hypotension related to hypovolemic shock includes: <ul><li>Volume infusion </li></ul><ul><li>Vaso...
Which of the following will produce cold extremities? <ul><li>Cardiogenic shock </li></ul><ul><li>Anaphylactic shock </li>...
SaO 2 /Hb CO O 2  Utilization  Extraction & VO 2  Venous Return SvO 2 O 2  Delivery
Questions?
Upcoming SlideShare
Loading in …5
×

Cv ii patho pharm fall 11

2,575 views

Published on

Published in: Health & Medicine
0 Comments
8 Likes
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total views
2,575
On SlideShare
0
From Embeds
0
Number of Embeds
11
Actions
Shares
0
Downloads
70
Comments
0
Likes
8
Embeds 0
No embeds

No notes for slide
  • It goes back to this simple cartoon of oxygen transport and venous oxygen delivery: To understand SvO2, we also make analogy of oxygen transport with this cartoon of the choo-choo train. The lungs load each hemoglobin with 4 oxygen molecules. Oxygen content is 20% of total volume. Given a cardiac output of 5 L/min, Oxygen delivery can be achieved at 1000 mL/min (DO2 = CO x CaO2). At the tissue level, Oxygen extraction is a ratio of oxygen consumed (VO2 = 250 mL/min) to the amount delivered (DO2), O 2 ER = VO2/DO2 = 250/1000 = 25% (normal). Thus 75% of oxygen delivered is returned to the venous side, i.e. normal SvO2 = 75%. Oxygen consumption (VO2) is a function of cardiac output and the difference between arterial (Hb x SaO2 x 13.4) and venous oxygen content (Hb x SvO2 x 13.4). Given the same CO and Hb, VO2 is analogous to the difference between arterial and venous oxygenation. For example, 1 Hb will deliver 4 oxygen molecules to the tissue -&gt; 1 oxygen molecule is consumed (VO2) by the tissue + 3 oxygen molecules are returned to the venous outflow.
  • A 38-year-old man was scheduled to undergo invasive coronary angiography after cardiac scintigraphy revealed silent ischemia of the anterior myocardial wall. He was a smoker and had no other medical problems apart from occasional atypical chest pain. Coronary angiography showed chronic total occlusion of the proximal part of the left anterior descending coronary artery (LAD), clinically insignificant atherosclerotic plaque in the right coronary artery, and collateral circulation to the distal portion of the LAD. Treatment with a beta-blocker was begun, and the patient underwent multislice computed tomography (CT) of the coronary arteries 1 month later to better assess the distal part of the LAD. CT showed tight bifocal stenoses in the first segment of the right coronary artery (Panel A). The patient was asymptomatic, but because coronary-artery spasm was strongly suspected, multislice CT was repeated 1 week later, with the use of intravenous isosorbide dinitrate as a vasodilator, and showed no stenoses in the right coronary artery (Panel B). The patient underwent successful coronary-artery bypass in which the left internal thoracic artery was anastomosed to the LAD, and he was doing well 1 year later. These findings show the ability of multislice CT to detect coronary-artery spasm in the right coronary artery and emphasize the utility of nitrate administration, as routinely performed during conventional invasive angiography.
  • It goes back to this simple cartoon of oxygen transport and venous oxygen delivery: To understand SvO2, we also make analogy of oxygen transport with this cartoon of the choo-choo train. The lungs load each hemoglobin with 4 oxygen molecules. Oxygen content is 20% of total volume. Given a cardiac output of 5 L/min, Oxygen delivery can be achieved at 1000 mL/min (DO2 = CO x CaO2). At the tissue level, Oxygen extraction is a ratio of oxygen consumed (VO2 = 250 mL/min) to the amount delivered (DO2), O 2 ER = VO2/DO2 = 250/1000 = 25% (normal). Thus 75% of oxygen delivered is returned to the venous side, i.e. normal SvO2 = 75%. Oxygen consumption (VO2) is a function of cardiac output and the difference between arterial (Hb x SaO2 x 13.4) and venous oxygen content (Hb x SvO2 x 13.4). Given the same CO and Hb, VO2 is analogous to the difference between arterial and venous oxygenation. For example, 1 Hb will deliver 4 oxygen molecules to the tissue -&gt; 1 oxygen molecule is consumed (VO2) by the tissue + 3 oxygen molecules are returned to the venous outflow.
  • Beyond the basic definition, it is helpful to think of sepsis as a continuum: Beginning with a localized infection that triggers a systemic response, called SIRS. SIRS due to infection is sepsis. Once the patient experiences organ dysfunction due to sepsis, that patient has the clinical diagnosis of severe sepsis. Any acute organ dysfunction qualifies the patient for the diagnosis of severe sepsis. Several examples of potential organ systems are listed on the slide. If the cardiovascular organ dysfunction deteriorates into shock, then this is commonly referred to as septic shock. Septic shock is a form (subgroup) of severe sepsis. Infection + SIRS + Organ Dysfunction = Severe Sepsis
  • Dellinger P, et al: Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock 2008. Crit Care Med . 2008;36(1):296-327
  • Dellinger P, et al: Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock 2008. Crit Care Med . 2008;36(1):296-327
  • It goes back to this simple cartoon of oxygen transport and venous oxygen delivery: To understand SvO2, we also make analogy of oxygen transport with this cartoon of the choo-choo train. The lungs load each hemoglobin with 4 oxygen molecules. Oxygen content is 20% of total volume. Given a cardiac output of 5 L/min, Oxygen delivery can be achieved at 1000 mL/min (DO2 = CO x CaO2). At the tissue level, Oxygen extraction is a ratio of oxygen consumed (VO2 = 250 mL/min) to the amount delivered (DO2), O 2 ER = VO2/DO2 = 250/1000 = 25% (normal). Thus 75% of oxygen delivered is returned to the venous side, i.e. normal SvO2 = 75%. Oxygen consumption (VO2) is a function of cardiac output and the difference between arterial (Hb x SaO2 x 13.4) and venous oxygen content (Hb x SvO2 x 13.4). Given the same CO and Hb, VO2 is analogous to the difference between arterial and venous oxygenation. For example, 1 Hb will deliver 4 oxygen molecules to the tissue -&gt; 1 oxygen molecule is consumed (VO2) by the tissue + 3 oxygen molecules are returned to the venous outflow.
  • As discussed in the previous slide, S v O 2 reflects the amount of oxygen remaining in the blood after the tissues have extracted the needed amount of oxygen. S v O 2 represents the difference between oxygen delivery (DO 2 ) and oxygen consumption (VO 2 ). The entire process can be described as follows: Oxygen loading onto hemoglobin occurs in the lungs (S a O 2 ). The oxygen on Hb is delivered by blood flow (CO) to the tissues. At the tissue level oxygen is removed and utilized (VO 2 ). S v O 2 reflects the difference between oxygen delivery (CO, S a O 2 , Hb) and oxygen consumption (VO 2 ).
  • Cv ii patho pharm fall 11

    1. 1. Disorders of Cardiac Function NURS 315/501 Kathryn T. Von Rueden RN, MS, FCCM University of Maryland School of Nursing
    2. 2.
    3. 3. Global Tissue Oxygenation Made Ridiculously Simple SvO2 = 75% 25% Venous Oxygen Delivery Arterial Oxygen Delivery Oxygen Consumption 100%
    4. 4. Coronary Circulation
    5. 5. Cardiac Conduction System <ul><li>Conduction system stimulates the myocardium to contract & pump blood </li></ul><ul><li>Conduction system usually controls the rhythm of the heart. </li></ul><ul><li>Heart has two conduction systems </li></ul><ul><ul><li>One controls atrial activity </li></ul></ul><ul><ul><li>One that controls ventricular activity </li></ul></ul>
    6. 6. Anatomy of the Conduction System SA Node AV Node Bundle of His Bundle branches Purkinje fibers Porth, 2007, Essentials of Pathophysiology, 2 nd ed., Lippincott, p. 331.
    7. 7. SA Node <ul><li>Pacemaker of the heart </li></ul><ul><li>Impulses originate here </li></ul><ul><li>Located in posterior wall RA </li></ul><ul><li>Fires at 60 -100 bpm </li></ul>
    8. 8. AV Node <ul><li>Connects the atria & ventricles, provides one way conduction </li></ul><ul><ul><li>Would beat independently </li></ul></ul><ul><li>Fires at 40 -60 bpm </li></ul><ul><li>Can assume pacemaker function if SA fails to discharge </li></ul>
    9. 9. Purkinjie Fibers <ul><li>Supplies the ventricles </li></ul><ul><li>Large fibers, rapid conduction for swift & efficient ejection of blood from heart </li></ul><ul><li>Fire 15-40 bpm </li></ul><ul><li>Assume pacemaker of ventricles if AV fails </li></ul><ul><li>HR reflects intrinsic firing of these structures </li></ul>
    10. 10. Action Potentials (AP) <ul><li>Stimulus </li></ul><ul><li> excitable tissues (muscle & conduction system) </li></ul><ul><li> evokes an AP characterized by a sudden change in voltage resulting from transient depolarization & then repolarization. </li></ul><ul><li>AP’s are electrical currents involving the movement/flow of electrically charged ions at level of cell membrane. </li></ul><ul><li>AP’s are conducted thru-out the heart, responsible for initiating each cardiac contraction. </li></ul>
    11. 11. SLOW SA & AV Nodes FAST Purkinje Fiber & Muscle
    12. 12. Cardiac Action Potentials <ul><li>3 types of membrane ion channels that contribute to voltage changes during the phases of the AP </li></ul><ul><ul><li>Fast Na + channels </li></ul></ul><ul><ul><ul><li>Rapid depolarization of muscles </li></ul></ul></ul><ul><ul><li>Slow Na + channels </li></ul></ul><ul><ul><ul><li>Pacemaker activity (SA, AV) </li></ul></ul></ul><ul><ul><li>Potassium channels </li></ul></ul><ul><ul><ul><li>Speedy repolarization </li></ul></ul></ul>
    13. 13. Three Phases of AP <ul><li>Resting </li></ul><ul><ul><li>Membrane is relatively permeable to K + , but much less so to Na + </li></ul></ul><ul><li>Depolarization </li></ul><ul><ul><li>Cell membrane becomes permeable to Na + </li></ul></ul><ul><ul><li>Na + enters cell, IC more + </li></ul></ul><ul><li>Repolarization </li></ul><ul><ul><li>Outward flow of positive charges, mainly K + </li></ul></ul><ul><ul><li>IC is more negative </li></ul></ul><ul><ul><li>Assisted by Na + -K + pump </li></ul></ul>
    14. 14. Cardiac Muscle Cell Firing <ul><li>Cells begin with a negative charge: resting membrane potential </li></ul><ul><li>Calcium leak lets Ca 2+ diffuse in, making the cell more positive </li></ul>Threshold potential Resting membrane potential Calcium leak
    15. 15. Cardiac Muscle Cell Firing (cont.) <ul><li>At threshold potential, more Na + channels open </li></ul><ul><li>Na + rushes in, making the cell very positive: depolarization </li></ul><ul><li>Action potential: the cell responds (e.g. by contracting) </li></ul>Threshold potential Resting membrane potential Action potential Calcium leak
    16. 16. Cardiac Muscle Cell Firing (cont.) <ul><li>K + channels open </li></ul><ul><li>K + diffuses out, making the cell negative again, but Ca 2+ channels are still allowing Ca 2+ to enter </li></ul><ul><li>The cell remains positive: plateau </li></ul>Threshold potential PLATEAU Action potential Calcium leak
    17. 17. Cardiac Muscle Cell Firing (cont.) <ul><li>During plateau , the muscle contracts strongly </li></ul><ul><li>Then the Ca 2+ channels shut and it repolarizes </li></ul>Threshold potential PLATEAU Action potential Calcium leak
    18. 18. Cardiac Action Potentials <ul><li>Unlike nerve cells, cardiac cells have five phases in their action potential </li></ul><ul><ul><li>Phase 4 – the resting membrane potential. </li></ul></ul><ul><ul><li>Phase 0 – there is rapid depolarization </li></ul></ul><ul><ul><li>Phase 1 – there is a short repolarization (only observed in ventricular muscle) </li></ul></ul><ul><ul><li>Phase 2 – the membrane potential remains depolarized in a plateau </li></ul></ul><ul><ul><li>Phase 3 – the membrane potential becomes repolarized. </li></ul></ul><ul><li>The characteristics of the phases are different in nodal tissues of the heart when compared with heart muscle cells or Purkinje fibers. </li></ul>
    19. 19. Cardiac Muscle Action Potential 5 Phases Phase 0 : Upstroke, rapid depolarization Phase 1: Early, short repolarization Seen only in ventricular mus cle Phase 2: Plateau phase; membrane potential remains depolarized Phase 3: Final rapid repolarization Phase 4: Resting, diastolic repolarization ** Unlike nerve cells, cardiac cells have 5 phases in their action potential.
    20. 20. Cardiac Muscle Cell Contraction <ul><li>During Phase 2, the plateau, calcium ion enters the muscle cell, causing it to contract strongly. </li></ul><ul><li>The strength of contraction is directly proportional to the number of calcium ions that enter the cell. </li></ul><ul><li>Calcium channel opening is controlled by voltage and by beta 1 receptors in the ventricular myocardium. </li></ul>
    21. 21. Lehne 5 th ed Figure 47-2 Myocardium & His-Purkinje System SA Node & AV Node <ul><li>Why are action potentials important? </li></ul><ul><li>Source of </li></ul><ul><ul><li>dysrhythmias </li></ul></ul><ul><li>Targets of </li></ul><ul><ul><li>drug action </li></ul></ul>
    22. 22. Cardiac Conduction & Rhythm Disorders
    23. 23. ECG: Relationship to Action Potential <ul><li>Electrical events recorded on ECG </li></ul><ul><li>Electrical events precede mechanical events; know what they represent! </li></ul><ul><ul><li>P </li></ul></ul><ul><ul><li>QRS </li></ul></ul><ul><ul><li>T </li></ul></ul>
    24. 24. Lehne 5 th ed Figure 47-3 Electrical event precedes mechanical event !!!
    25. 25. Porth 2007, Figure 16-12 P wave PR Interval QRS complex T wave: Repolarization
    26. 26. Disorders of Cardiac Rhythm and Conduction : 2 Types <ul><li>Dysrhythmias (or arrhythmias) </li></ul><ul><ul><li>Term used to describe disorders of cardiac rhythm </li></ul></ul><ul><ul><li>Occur in healthy and non-healthy </li></ul></ul><ul><ul><li>Interfere with heart’s pumping ability </li></ul></ul><ul><li>Disorders of impulse conduction </li></ul>
    27. 27. Disorders of Cardiac Rhythm and Conduction <ul><li>2 types of disorders of the cardiac conduction system </li></ul><ul><ul><li>1. Disorders of rhythm </li></ul></ul><ul><ul><li>2. Disorders of impulse conduction </li></ul></ul><ul><li>Dysrhythmias (or arrhythmias) </li></ul><ul><ul><li>Term used to describe disorders of cardiac rhythm </li></ul></ul><ul><ul><li>Occur in healthy and non-healthy </li></ul></ul><ul><ul><li>Interfere with heart’s pumping ability </li></ul></ul>
    28. 28. Causes <ul><li>Congenital defects in conduction system </li></ul><ul><li>Degenerative changes </li></ul><ul><li>Ischemia and MI </li></ul><ul><li>Fluid/electrolyte imbalances </li></ul><ul><li>Drugs </li></ul>
    29. 29. Sinus Node Rhythms <ul><li>Normal Sinus Rhythm </li></ul><ul><ul><li>P wave precedes each QRS, RR intervals reg, rate 60-100 </li></ul></ul><ul><li>Sinus Bradycardia </li></ul><ul><li>P before QRS, RR regular, rate </li></ul><ul><li>< 60, slowing of conduction thru AV node (Vagal, PNS) </li></ul><ul><li>Sinus Tachycardia </li></ul><ul><li>P before QRS, RR regular, </li></ul><ul><li>rate > 100. Enhanced </li></ul><ul><li>automaticity r/t SNS activation (fever, exercise, stress) </li></ul>
    30. 30. Lehne 5 th ed Figure 47-2 Myocardium & His-Purkinje System SA Node & AV Node Class II Antidysrhythmic
    31. 31. Class II Antidysrhythmic Beta Blockers <ul><li>Depress Phase 4 in depolarization </li></ul><ul><li>Nonselective: Carvedilol, Propranolol: </li></ul><ul><li>Block beta 1 & 2 receptors </li></ul><ul><li>Cardioselective: Metropolol, Esmolol: </li></ul><ul><li>Block beta 1 only </li></ul><ul><li>Mechanism of Action: </li></ul><ul><ul><li>(-) Inotrope </li></ul></ul><ul><ul><li>(-) Chronotrope – SLOW the heart rate! </li></ul></ul><ul><ul><li>(-) Dromotrope </li></ul></ul>
    32. 32. Class II Antidysrhythmic Beta Blockers <ul><li>ECG </li></ul><ul><ul><li>Prolong PR & bradycardia </li></ul></ul><ul><li>Pharmacotherapeutics: </li></ul><ul><ul><li>PSVT </li></ul></ul><ul><ul><li>Angina </li></ul></ul><ul><ul><li>AMI </li></ul></ul><ul><ul><li>Hypertension (HTN) ( not esmolol) </li></ul></ul><ul><ul><li>Heart Failure (HF) (carvedilol, metoprolol) </li></ul></ul>See Lehne Table 18-2 & 18-3
    33. 33. Beta Blocker: Adverse effects <ul><li>Hypotension </li></ul><ul><li>Syncope </li></ul><ul><li>Precipitate HF </li></ul><ul><li>Bradycardia </li></ul><ul><li>AV block </li></ul><ul><li>Sinus arrest </li></ul><ul><li>Bronchospasm (non-selective beta blockers) </li></ul><ul><li>Rebound cardiac excitation (if abruptly stopped) </li></ul>
    34. 34. Beta Blocker Administration (remember from last week) Drug Route ½ Life (hrs) Indication Esmolol IV ONLY! 0.15 Dysrh, angina Metoprolol IV, PO 3-7 Dysrh, angina, AMI, HF, HTN Atenolol IV, PO 6-9 Dysrh, angina, AMI Carvedilol PO 5-11 Angina, AMI, HF, HTN Propanolol IV, PO 3-5 Dysrh, angina, AMI, HTN
    35. 35. Atrial Dysrhythmias Atrial Fibrillation : Chaotic & disorganized current. Atria are depolarizing without contracting (just quivering). Ventricular rhythm irregular. Only irregularly irregular rhythm. No discernable P waves.
    36. 36. A-Fib treatment: Digoxin <ul><li>A cardiac glycoside that is used for atrial fibrillation or atrial flutter. </li></ul><ul><li>Slows conduction in the AV node and thereby slows ventricular rate. </li></ul>
    37. 37. Digoxin <ul><li>Mechanism of Action: </li></ul><ul><li>Inhibits Na + -K + ATPase; more intracellular calcium available </li></ul><ul><ul><li> + inotrope </li></ul></ul><ul><li>Enhance vagal influence (SA & AV node effect) </li></ul><ul><ul><li> - chronotrope, - dromotrope </li></ul></ul><ul><li>Pharmacotherapeutics: </li></ul><ul><ul><li>Heart failure </li></ul></ul><ul><ul><li>Atrial flutter </li></ul></ul>
    38. 38. Lehne 6 th ed Figure 47-4
    39. 39. Digoxin: Pharmacokinetics Absorption 60 – 80% (tabs) 70 – 85% (elixir) 90 – 100% (caps) Metabolism Liver Half Life 5-7 DAYS to eliminate & T½ 1.5 days
    40. 40. Digoxin Administration Considerations <ul><li>PO or IV (mcg NOT mg) </li></ul><ul><ul><li>“ Digitalization” </li></ul></ul><ul><ul><li>IV loading dose </li></ul></ul><ul><li>Digoxin levels (0.5 - 1.1 ng/ml) </li></ul><ul><ul><li>VERY narrow therapeutic range </li></ul></ul><ul><ul><li>Digoxin immune FAB (antidote) for toxic levels ( > 2.0 ng/ml) </li></ul></ul><ul><ul><li>D/C drug until toxicity resolves </li></ul></ul>
    41. 41. Adverse effect & S/S digoxin toxicity <ul><ul><li>Digoxin induced dysrhythmias </li></ul></ul><ul><ul><ul><li>All types! </li></ul></ul></ul><ul><ul><ul><li>Bradycardia </li></ul></ul></ul><ul><ul><ul><li>AV block most common </li></ul></ul></ul><ul><ul><ul><li>Ventricular flutter/fib most dangerous </li></ul></ul></ul><ul><li>GI : Anorexia, N/V </li></ul><ul><li>CNS: Drowsiness/weakness, </li></ul><ul><li>Blurred vision/colored (yellow) halos </li></ul>
    42. 42.
    43. 43. Digoxin Contraindications & Precautions Contraindications Precautions 2 nd /3 rd degree heart block V. Fib/V. Tach Sick Sinus Syndrome Acute MI Renal insufficiency Hypokalemia Severe pulmonary disease
    44. 44. Digoxin Additional Considerations <ul><li>Potassium levels </li></ul><ul><li>Keep in 3.5 – 5.0 mEq/L range </li></ul><ul><ul><li>Digoxin competes with K + @ binding sites </li></ul></ul><ul><ul><li>Hyperkalemia  decreases digoxin effect </li></ul></ul><ul><ul><li>Diuretics may cause hypokalemia </li></ul></ul><ul><ul><li> digoxin toxicity </li></ul></ul>
    45. 45. Drug  Drug Interactions <ul><li>Reduce digoxin therapeutic effect </li></ul><ul><li>ACE-I & ARBs </li></ul><ul><ul><li>Increase potassium </li></ul></ul><ul><li>Additive digoxin effect </li></ul><ul><li>Sympathomimetics </li></ul><ul><ul><li>Increase contractility & HR </li></ul></ul><ul><ul><li>Increase risk of tachydysrhythmias </li></ul></ul><ul><li>Numerous interactions (Lehne Table 47-2) </li></ul>
    46. 46. Drug  Drug Interactions Increase risk of digoxin toxicity <ul><li>Calcium channel blockers (verapamil) </li></ul><ul><ul><li>Increase serum dig level </li></ul></ul><ul><ul><li>Decrease HR </li></ul></ul><ul><ul><li>Bradydysrhythmias or complete heart block </li></ul></ul><ul><li>Diuretics may reduce potassium levels </li></ul><ul><ul><li>Increase risk of dig-induced dysrhythmias </li></ul></ul><ul><li>Herbal interactions increase metabolism </li></ul>
    47. 47. Digoxin: Nursing Implications Apical pulse for 1 min. & document Monitor ECG Monitor potassium & dig levels
    48. 48. A-Fib, PSVT Treatment Class IV Antidysrhythmic Calcium Channel Blockers <ul><li>Verapamil, diltazem </li></ul><ul><li>Mechanism of Action: </li></ul><ul><ul><li>Inhibits calcium influx during depolarization </li></ul></ul><ul><ul><li>Depresses phase 4 of depolarization </li></ul></ul><ul><ul><li>Prolongs phases 1 & 2 of depolarization </li></ul></ul>
    49. 49. Lehne 5 th ed Figure 47-2 Myocardium & His-Purkinje System SA Node & AV Node
    50. 50. Class IV Antidysrhythmic Calcium Channel Blockers (verapamil, diltiazem) <ul><li>3 effects on heart </li></ul><ul><li>Slow SA node automaticity  slow HR </li></ul><ul><li>Delay AV node conduction  prolong PR </li></ul><ul><li> myocardial contractility   CO </li></ul><ul><li>Note: same effects as Beta Blockers!!!!! </li></ul><ul><li>Pharmacotherapeutics : </li></ul><ul><ul><li>PSVT Atrial Fib/Flutter (slow ventricular rate) </li></ul></ul><ul><ul><li>Angina Hypertension </li></ul></ul><ul><ul><li>Note: not effective for ventricular dysrhythmias !! </li></ul></ul>
    51. 51. Verapamil & Diltiazem Adverse Effects ( Remember from last week) <ul><li>Cardiac: </li></ul><ul><li>Bradycardia </li></ul><ul><li>AV block </li></ul><ul><li>Decreased myocardial contractility  decreased cardiac output </li></ul><ul><li>General: </li></ul><ul><li>Dizziness </li></ul><ul><li>Facial Flushing </li></ul><ul><li>Headache </li></ul><ul><li>Peripheral edema </li></ul><ul><li>Decreased </li></ul><ul><li>GI motility </li></ul>
    52. 52. Disorders of Atrioventricular Conduction 1st degree AV block: Slightly prolonged PR interval; ALL atrial impulses are conducted to ventricles; asymptomatic. 2nd degree AV block: Not all atrial impulses are conducted to ventricles, see some P waves, not followed by QRS. Can be very symptomatic. 3rd degree AV block = complete AV block: Conduction link between atria & ventricles lost, each controlled by independent pacemakers. Atria continue at their rate, ventricles contract at their rate (30-40 bpm).
    53. 53. Case study: Digoxin toxicity Serum dig level = 1.7 ng.ml (0.5-1.1 desired) 3 rd degree AV Block Temporary pacemaker inserted, SR  100% paced
    54. 54. Complete A-V block with 100% atrio-ventricular pacing Atrial Pacing spike Ventricular Pacing spike P QRS
    55. 55. Ventricular Dysrhythmias: More Serious! PVC: Ventricles contract prematurely. W/ a PVC, diastolic volume is insufficient for ejection of blood into arterial system. Therefore, no or weak pulse palpated. Few/day = OK, More/minute, the worse (>6). Common post MI, SNS activity,  K+, hypoxia. V-Tachycardia: rhythm originates below Bundle of His, in ventricular muscle. Wide, tall QRS complexes. Stops spontaneously or continue. Dangerous rhythm,  diastolic filling time   CO. Can cause Cardiac Arrest V-Fib: ventricle quivers but does NOT contract!  NO cardiac output , and no pulses; Cardiac Arrest!! grossly disorganized pattern.
    56. 56. Lehne 5 th ed Figure 47-2 Myocardium & His-Purkinje System SA Node & AV Node Class I Antidysrhythmic
    57. 57. Class 1B: Lidocaine Ventricular Dysrhthmias
    58. 58. Class 1B: Lidocaine <ul><li>Effect on Heart & ECG </li></ul><ul><ul><li>Blocks Na+ channels  slow conduction thru atria, ventricles, HIS-Purkinje </li></ul></ul><ul><ul><li>Reduces automaticity </li></ul></ul><ul><ul><li>Accelerates repolarization (shortens action potential) </li></ul></ul><ul><li>No anticholinergic effect </li></ul><ul><li>No change in ECG </li></ul>
    59. 59. Lidocaine: Precautions & Adverse Effects <ul><li>Metabolized by Liver </li></ul><ul><li>Therapeutic range 1.5 – 5.0 microgm/ml </li></ul><ul><li>Adverse CNS Effects: </li></ul><ul><ul><li>Drowsiness, confusion, paresthesia </li></ul></ul><ul><li>Toxicity: </li></ul><ul><ul><li>Convulsions & respiratory arrest </li></ul></ul>
    60. 60. Lidocaine: Administration <ul><li>IV Push </li></ul><ul><ul><li>50-100mg (1mg/kg) </li></ul></ul><ul><li>Infusion </li></ul><ul><ul><li>1-4mg/min </li></ul></ul><ul><ul><li>Diluted in D5W </li></ul></ul><ul><li>Special Considerations: </li></ul><ul><ul><li>Use for as short a time as possible </li></ul></ul><ul><ul><li>Reduce dosage in pts with liver disorders </li></ul></ul>
    61. 61. Class III Antidysrhythmic <ul><li>Potassium Channel Blockers: Amiodarone </li></ul><ul><li>Approved for VT & VF </li></ul><ul><li>Delay repolarization </li></ul><ul><li>  Prolongs action potential & refractory period </li></ul><ul><li>  Increases PR & QT intervals </li></ul>Initial  catecholamine release  brief exacerbation of dysrhythmias  block catecholamine release  vasodilation / hypotension
    62. 62. Lehne 5 th ed Figure 47-2 Myocardium & His-Purkinje System SA Node & AV Node Class III Antidysrhythmic
    63. 63. Non-Pharmacologic Treatment of Dysrhythmias <ul><li>Cardioversion </li></ul><ul><ul><li>Atrial fib </li></ul></ul><ul><ul><li>V-tach </li></ul></ul><ul><li>Defibrillation </li></ul><ul><ul><li>V-fib </li></ul></ul>                                                     
    64. 64. Automated External Defibrillator <ul><li>Cardiac Arrest, AED “interrogates” rhythm. </li></ul><ul><li>Tells user what to do, eg “Shock Now” </li></ul><ul><li>Delivers shock for V-tach or V-fib. </li></ul>
    65. 65. Non-Pharmacologic Treatment of Dysrhythmias <ul><li>Implantable Cardioverter/Defibrillator </li></ul><ul><ul><li>Like a pacemaker </li></ul></ul><ul><ul><li>Monitors & analyzes rhythm </li></ul></ul><ul><ul><li>Delivers shock to terminate V-tach, V-fib </li></ul></ul><ul><li>Radiofrequency Catheter Ablation </li></ul><ul><ul><li>Cardiac cath & electrophysiologic test </li></ul></ul><ul><ul><li>Identify cardiac tissue site which causes dysrhythmia </li></ul></ul><ul><ul><li>RF energy delivered to destroy the tissue (remember, you can’t pace meatloaf) </li></ul></ul>
    66. 66. Antidysrhythmic Drugs: Summary <ul><li>Class I </li></ul><ul><ul><li>Depress phase 0 in depolarization </li></ul></ul><ul><ul><li>Block sodium channels </li></ul></ul><ul><li>Class II </li></ul><ul><ul><li>Depress phase 4 in depolarization </li></ul></ul><ul><ul><li>Block beta 1 & 2 adrenergic receptors </li></ul></ul><ul><ul><ul><li>HR Contractility </li></ul></ul></ul>
    67. 67. <ul><li>Class III </li></ul><ul><ul><li>Prolong phase 3 (repolarization) </li></ul></ul><ul><li>Class IV </li></ul><ul><ul><li>Depresses phase 4 depolarization </li></ul></ul><ul><ul><li>Prolongs phases 1 & 2 repolarization </li></ul></ul>Antidysrhythmic Drugs: Summary
    68. 68. Management of Cardiac Dysrhythmias REMEMBER: Many drugs used to treat dysrhythmias also may worsen them or cause new ones!
    69. 69. Coronary Heart Disease & Acute Myocardial Infarction (MI or AMI)
    70. 70. Coronary Circulation <ul><li>Two main coronary arteries arise from coronary sinus (above aortic valve) </li></ul><ul><li>Primary factor responsible for perfusion coronary arteries is BP in aorta </li></ul><ul><li> s aortic pressure -> </li></ul><ul><li> s coronary blood flow </li></ul>
    71. 71. Coronary Circulation LV LV
    72. 72.
    73. 73. Ischemic Heart Disease a.k.a Coronary Heart Disease a.k.a Coronary Artery Disease Angina Myocardial Infarction
    74. 74. Coronary Heart Disease <ul><li>Heart disease caused by impaired coronary blood flow (atherosclerosis) </li></ul><ul><li>Cause angina, dysrhythmias, conduction defects, heart failure, sudden death, myocardial infarction (“heart attack”) </li></ul><ul><li>If blood flow is temporarily inadequate (due to increased oxygen demand), ischemia produces pain (angina). </li></ul><ul><li>Myocardial Infarction is myocardial cell/tissue death due to oxygen starvation </li></ul>
    75. 75. Assessment of Coronary Blood Flow <ul><li>ECG </li></ul><ul><li>Exercise Stress Testing </li></ul><ul><li>Pharmacologic Stress Testing </li></ul><ul><li>Nuclear Imaging </li></ul><ul><li>Cardiac Catheterization /Coronary angiography </li></ul>
    76. 76. Collateral Circulation <ul><li>With gradual occlusion of large coronary vessels, the smaller collateral vessels  in size and provide alternative channels for blood flow </li></ul><ul><li>One of the reasons CHD does not produce symptoms until it is far advanced is that the collateral channels develop at the same time the atherosclerotic changes are occurring. </li></ul>
    77. 77. Collateral Circulation
    78. 78. Pathogenesis of CAD: Atherosclerosis <ul><li>Most common cause of CAD </li></ul><ul><li>Plaque disruption is most frequent cause of MI, sudden death </li></ul><ul><li>Can affect one or all 3 major coronary arteries/branches </li></ul>
    79. 79. Plaque <ul><li>Plaques typically do not occlude the whole coronary artery but produce a narrowing that restricts blood flow. </li></ul><ul><ul><li>In times of increased oxygen demand, such as with exercise, the restricted blood flow may produce ischemia in cells supplied by that artery. </li></ul></ul><ul><ul><li>This produces the pain of angina. </li></ul></ul><ul><li>A plaque may become unstable and rupture, causing a clot to form which may completely occlude the artery. </li></ul><ul><ul><li>Occlusion of the artery causes death of the cardiac cells downstream that are supplied by that artery. </li></ul></ul><ul><ul><li>When the cells die, that is an infarction – hence the name myocardial infarction. </li></ul></ul>
    80. 80. Atherosclerosis in Coronary Artery <ul><li>Plaque rupture & disruption of atheroma  </li></ul><ul><li> lipid core/contents exposed to blood </li></ul><ul><li> platelet aggregation  coagulation cascade </li></ul><ul><li> fibrin clot </li></ul><ul><li> thrombosis, vasospasm </li></ul><ul><li> myocardial ischemia </li></ul><ul><li> Coronary arteries unable to supply blood to meet metabolic demands of the heart </li></ul>
    81. 81. Review of Terms Related to CHD <ul><li>Angina: symptomatic paroxysmal chest pain or pressure sensation associated with transient myocardial ischemia </li></ul><ul><li>Stable angina: Occurs with exertion or stress </li></ul><ul><li>Variant or vasospastic angina: Occurs during rest or with minimal activity (nocturnal, Prinzmetal’s) </li></ul><ul><li>Silent myocardial ischemia : Occurs in the absence of anginal pain </li></ul><ul><li>Unstable angina : Symptoms at rest lasting >20 mins., marked limitations of ordinary activity (walking 1–2 blocks, climbing a flight of stairs), recent acceleration in anginal signs </li></ul><ul><li>AMI: Acute myocardial infarction (STEMI or NSTEMI) </li></ul>
    82. 82.
    83. 83.
    84. 84.
    85. 85.
    86. 86. Plaque Rupture <ul><li>Spontaneous </li></ul><ul><ul><li>SNS activation  BP,  HR,  contraction </li></ul></ul><ul><ul><li>Triggering event (stress: emotional, physical) </li></ul></ul><ul><li>Diurnal </li></ul><ul><ul><li>First hour of arising </li></ul></ul><ul><ul><li>SNS “surge” on arising </li></ul></ul><ul><li>SNS major player </li></ul><ul><ul><li>Beta-adrenergic blockers </li></ul></ul>
    87. 87. “ Severe” coronary stenosis and vulnerable plaques co-exist Califf, Atlas of Heart Diseases 2001
    88. 88. Ischemia, Injury, & Infarction <ul><li>3 Zones of Damage </li></ul><ul><li>Infarction = Necrosis </li></ul><ul><li>-MI, dead cells </li></ul><ul><li>Injury </li></ul><ul><li>-some recovery possible </li></ul><ul><li>Ischemia </li></ul><ul><li>- full recovery possible </li></ul>
    89. 89. Zones of Tissue Damage <ul><li>Goal is to limit the area of necrosis (infarction) ! </li></ul><ul><li>Necrotic myocardial cells are gradually replaced with scar tissue </li></ul><ul><li>Scar tissue cannot contract or conduct action potentials </li></ul>
    90. 90. An Acute MI (AMI) Leaves Behind an Area of Yellow Necrosis
    91. 91. Pathologic Changes <ul><li>Ischemic areas cease to function within minutes </li></ul><ul><li>Irreversible damage/death to myocardial cells occurs within 20-40 minutes </li></ul><ul><li>Early reperfusion (20min) after onset of ischemia can prevent necrosis, prevent further ischemia and necrosis </li></ul>
    92. 92. Pathologic Changes <ul><li>Extent of infarct depends on : </li></ul><ul><li>location </li></ul><ul><li>extent of occlusion </li></ul><ul><li>amount of heart tissue supplied by vessel, duration of occlusion </li></ul><ul><li>metabolic needs of the affected tissue </li></ul><ul><li>extent of collateral circulation </li></ul>
    93. 93. Pathologic Changes <ul><li>Transmural infarct </li></ul><ul><ul><li>Full thickness of ventricular wall, </li></ul></ul><ul><ul><li>Occurs with obstruction of a single artery; </li></ul></ul><ul><ul><li>May involve RV, LV and/or IV septum </li></ul></ul><ul><li>Subendocardial infarct </li></ul><ul><ul><li>Involve inner 1/3 to 1/2 ventricular wall, </li></ul></ul><ul><ul><li>May occur with severely narrowed arteries or with occlusion of a very small artery </li></ul></ul>Porth, 2007, Essential of Pathophysiology, 2 nd ed., Lippincott, p. 328.
    94. 94.
    95. 95. Chest Pain Assessment <ul><li>P - Provocation </li></ul><ul><li>Q - Quality </li></ul><ul><li>R – Region/Radiation </li></ul><ul><li>S - Severity </li></ul><ul><li>T – Timing </li></ul>
    96. 96. Categories (PQRST) <ul><li>Angina that occurs with stress (physical/emotional) </li></ul><ul><ul><li>Relieved within minutes by rest or NTG? </li></ul></ul><ul><li>Angina that occurs with rest </li></ul><ul><li>Is of new onset </li></ul><ul><li>Increasing intensity </li></ul> risk for MI
    97. 97.
    98. 98. Stable Angina <ul><li>Fixed coronary obstruction </li></ul><ul><li> 0 2 Demand   0 2 supply  pain </li></ul><ul><ul><li>Physical/emotional stress, cold </li></ul></ul><ul><li>Provoked by stressor </li></ul><ul><ul><li>Relieved with rest/NTG </li></ul></ul><ul><li>Not everyone with CHD has angina </li></ul><ul><ul><li>Sedentary lifestyle (couch potatoes), development of collateral circulation, altered perception pain </li></ul></ul>
    99. 99. Angina Typically precordial, substernal Usual distribution of pain Less common sites of pain distribution
    100. 100. Variant or Vasospastic Angina <ul><li>“ Prinzmetal’s angina” </li></ul><ul><li>Due to coronary artery spasms </li></ul><ul><li>Occurs during rest or with minimal exertion, frequently nocturnal </li></ul><ul><li>Mechanism uncertain </li></ul><ul><ul><li>?SNS activation, VSM Ca ++ channel dysfunction, imbalance of endothelial cell vasodilating/constricting substances </li></ul></ul><ul><li>Dysrhythmias can occur </li></ul><ul><ul><li>Person usually aware; High risk sudden death </li></ul></ul>
    101. 101. Hamon M and Hamon M. N Engl J Med 2006;355:2236 A 38-year-old man was scheduled to undergo invasive coronary angiography after cardiac scintigraphy revealed silent ischemia of the anterior myocardial wall Variant or Vasospastic Angina
    102. 102. Acute Coronary Syndrome (ACS) NSTEMI STEMI Unstable or ruptured plaque
    103. 103. Acute Coronary Syndrome (ACS)
    104. 104. Unstable Angina <ul><li>Clinical syndrome of myocardial ischemia ranging between stable angina and MI </li></ul><ul><li>Usually d/t atherosclerotic plaque disruption, plt aggregation </li></ul><ul><li>Three presentations </li></ul><ul><ul><li>Symptoms at rest (> 20 minutes) </li></ul></ul><ul><ul><li>Severe, frank pain, new onset (< 1month) </li></ul></ul><ul><ul><li>More severe, prolonged, or frequent </li></ul></ul>
    105. 105. Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392 .
    106. 106. Acute Coronary Syndrome (ACS)
    107. 107. ST Segment Elevation <ul><li>ST segment elevations are indicative of myocardial damage or ischemia. </li></ul><ul><li>It may take some time (minutes to hours) for the changes to show up, and they may not be present in all EKG leads. </li></ul>Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 394 .
    108. 108. ECG : STEMI vs NSTEMI
    109. 109. Non ST Segment Elevation Myocardial Infarction (NSTEMI) How is this different from unstable angina or STEMI? Unstable angina , plaque disruption but no thrombus or occlusion of the coronary artery, therefore no myocardial cell death (no MI). NSTEMI , a thrombus partially occludes a coronary artery. Depending on the degree of occlusion and oxygen demand of downstream heart cells, there may be myocardial cell death (an MI) but insufficient to produce ST segment elevations.
    110. 110. Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392 .
    111. 111. ST Segment Elevation MI <ul><li>Characterized by ischemia of cardiac tissue </li></ul><ul><li>Area of infarction is determined by the coronary artery that is affected and by its distribution of blood flow </li></ul><ul><ul><li>40-50% of time - LAD </li></ul></ul><ul><ul><li>30-40% of time - RCA </li></ul></ul><ul><ul><li>15-20% of time - LCA </li></ul></ul>
    112. 112. Porth, 2007, Essentials of Pathophysiology, 2nd ed., Lippincott, p. 392 .
    113. 113. Diagnosis CHD and MI <ul><li>Good history & identification of risk factors </li></ul><ul><li>R/O Other causes of CP, eg GERD </li></ul><ul><li>ECG </li></ul><ul><li>Serum myocardial markers </li></ul><ul><li>Stress testing </li></ul><ul><li>Cardiac catheterization </li></ul>
    114. 114. “ Classic” Manifestations of MI <ul><li>Abrupt onset or progression of unstable, non-ST elevation </li></ul><ul><li>Pain is severe, crushing, “someone sitting on my chest” </li></ul><ul><li>Radiates to left arm, jaw, neck </li></ul><ul><li>MI pain is prolonged, not relieved by rest and/or NTG (unlike angina) </li></ul><ul><li>N/V, SNS activation   HR,  RR, diaphoresis, cool/clammy skin </li></ul>
    115. 115. ECG Changes <ul><li>T wave inversion </li></ul><ul><li>ST segment elevation </li></ul><ul><li>Abnormal Q wave </li></ul><ul><li>(may not appear immediately) </li></ul><ul><li>Changes can occur over time, depending on duration of ischemia (extent & location) </li></ul><ul><li>Changes may not be present in all leads – take 12-lead EKG </li></ul>
    116. 116. ST Segments <ul><li>1 st to change during ischemia or MI because myocardial repolarization is altered. </li></ul><ul><li>Ischemia reduces membrane potential and shorten duration of AP in ischemic area. </li></ul>
    117. 117. Abnormal Q Waves <ul><li>Develop because there is no depolarizing current conduction from necrotic tissue </li></ul><ul><li>May not appear immediately </li></ul><ul><li>Diagnostic of MI </li></ul><ul><li>Q waves are permanent after MI </li></ul>
    118. 118. Serum Markers for Ischemia & MI <ul><li>Necrotic cells release intracellular enzymes into blood stream </li></ul><ul><li>Measure these in blood, larger the number, the larger the amount of necrotic tissue </li></ul><ul><ul><li>CK-MB (Creatine-kinase-myocardial bands) </li></ul></ul><ul><ul><li>Troponin </li></ul></ul><ul><ul><li>C-reactive Protein </li></ul></ul>
    119. 119. CK-MB <ul><li>CK normal in all muscle cells, has 3 isoenzymes BB, MM, MB </li></ul><ul><li>CK-MB Creatine kinase -myocardial bands is cardiac specific </li></ul><ul><li>Elevated within 8 hours after MI </li></ul><ul><li>Returns to normal in 2-3 days </li></ul><ul><li>Nl ~ 24-195 IU/L </li></ul>
    120. 120. Troponin (TnC, TnI, TnT) <ul><li>Part of the actin-myosin filament </li></ul><ul><li>Rises within 3 hours after MI </li></ul><ul><li>Remains elevated 3-4 days, & up to 10 days </li></ul><ul><li>Diagnostic of MI; No change with ischemia </li></ul><ul><li>Nl ~ 0.4 ng/ml </li></ul>
    121. 121. C-Reactive Protein (CRP) <ul><li>Marker of chronic inflammation </li></ul><ul><li>Maybe a marker of risk </li></ul><ul><li>Identifies people before they are symptomatic </li></ul><ul><li>May guide preventative therapy in future </li></ul>
    122. 122. Cardiac Markers Hr 1 2 3 4 5 6 7 8 9 10 11 12 Day 2 3 4 5 Troponin CK-MB
    123. 123. NSTEMI Unstable angina No ECG  s Elevation of serum markers Unstable Angina Pain is severe No ECG  s No change in markers ACS No ST Elevation STEMI
    124. 124.
    125. 125. ACS Case Presentation 1 <ul><li>68 yr male; 3 mos. h/o progressive chest pain; day of adm, with minimal exertion </li></ul><ul><li>Risk factors : Smoking; HTN;  cholesterol; diabetes </li></ul><ul><li>Physical exam: normal </li></ul><ul><li>ECG : sinus rhythm; no ST or T-wave abnormalities </li></ul><ul><li>Biochemical markers at 10 hours : </li></ul><ul><li> CK = 58; </li></ul><ul><li> CKMB = <1 ng/ml; </li></ul><ul><li> Tn= 0.31 ng/ml </li></ul><ul><li>Not an MI !! </li></ul>
    126. 126. Management of Angina & CHD/AMI <ul><li>Goals: </li></ul><ul><li>Prevent or minimize infarction </li></ul><ul><li>Increase oxygen supply to myocardium </li></ul><ul><li>Decrease metabolic (oxygen) demands </li></ul><ul><li>Symptom relief </li></ul>
    127. 127. Management of Angina & CHD/AMI <ul><li>Treatment </li></ul><ul><ul><li>Non-pharmacologic: Percutaneous Coronary Intervention (PCI), life style modifications </li></ul></ul><ul><ul><li>Pharmacologic: anti-platelet drugs, beta blockers, nitrates </li></ul></ul>
    128. 128. Acute Management: Reperfusion <ul><li>PTCA/PCI </li></ul><ul><ul><li>ASAP </li></ul></ul><ul><ul><li>With or without thrombolytics </li></ul></ul><ul><ul><li>Often includes placement of a stent </li></ul></ul><ul><li>CABG </li></ul><ul><li>Thrombolytics </li></ul><ul><li>- Tissue plasminogen activator (t-PA) </li></ul><ul><li>- Streptokinase </li></ul><ul><li>- Urokinase </li></ul><ul><li>Reteplase </li></ul><ul><ul><li>(modification of t-PA) </li></ul></ul>
    129. 129. Reperfusion McCance 5 th Ed, 2006 Figure 30-2
    130. 130. Reperfusion – Balloon Angioplasty, Possibly with Stenting Copyright © 2005 Nucleus Communications, Inc. All rights reserved. www.nucleusinc.com http://www.orbusneich.com/patients/genous/treatment/stenting/?PHPSESSID=d3bf5eb0eed5f6a353d73c
    131. 131. Complication of PCI N Engl J Med 2011;364:453-64.
    132. 132. Administration of Thrombolytic Therapy Must be Done Promptly Giugliano & Braunwald, Circulation 2003;108;2828-2830 IRA = infarct-related artery
    133. 133. PCI (angioplasty ± stenting) must be done promptly Nallamothu B et al. N Engl J Med 2007;357:1631-1638
    134. 134. Emergency Pain Relief <ul><li>Morphine Sulfate </li></ul><ul><li>Venodilation </li></ul><ul><ul><li>Reduces preload & cardiac work </li></ul></ul><ul><li>“ Modest” arterial vasodilation </li></ul><ul><ul><li>Reduces afterload & cardiac work </li></ul></ul>
    135. 135. <ul><li>Nitroglycerin </li></ul><ul><ul><li>Angina </li></ul></ul><ul><ul><li>Acute myocardial infarction </li></ul></ul><ul><li>Mechanism of Action: </li></ul><ul><ul><li>Prevents vasospasm of coronary arteries </li></ul></ul><ul><ul><li>Venodilator  Decreases preload </li></ul></ul><ul><ul><li>  Decreases LVEDV </li></ul></ul><ul><ul><li>  Decreases cardiac work </li></ul></ul>
    136. 136. Nitroglycerin Lehne, 2006 Tables 50-3 and 50-4 Purpose/Onset Administration Duration SL Acute angina 1 – 3 min 0.3 – 0.6 mg prn 30 - 60 min IV Acute, unstable 1-3 min <ul><li>5 microgm/min then increase </li></ul><ul><li>Special tubing </li></ul><ul><li>Glass bottles </li></ul><ul><li>Increased tolerance </li></ul>3 - 5 min
    137. 137. Nitroglycerin Pharmacokinetics <ul><li>Metabolized in the liver </li></ul><ul><li>Excreted by liver & kidneys </li></ul><ul><li>Use with caution in patients with liver or kidney disease </li></ul><ul><li>Onset & duration of action administration route dependent </li></ul>
    138. 138. Nitroglycerin Contraindications <ul><li>Severe hypotension </li></ul><ul><li>Increased ICP </li></ul><ul><li>Cerebral hemorrhage </li></ul><ul><li>Severe anemia </li></ul>
    139. 139. Nitroglycerin Drug  Drug Interactions <ul><li>Alcohol </li></ul><ul><ul><li>SEVERE hypotension; CV collapse </li></ul></ul><ul><li>Heparin </li></ul><ul><ul><li>Decreased anticoagulation </li></ul></ul><ul><li>Lithium </li></ul><ul><ul><li>Possible lithium toxicity </li></ul></ul><ul><li>Fentanyl </li></ul><ul><ul><li>SEVERE hypotension; Increased fluid requirements </li></ul></ul>
    140. 140. Chronic HD & Angina Management <ul><li>Nitrates </li></ul><ul><li>Beta Blockers </li></ul><ul><li>Calcium channel blockers </li></ul>
    141. 141. Nitrates: Chronic Angina Lehne, 2006 Tables 50-3 and 50-4 Purpose/Onset Administration Duration Oral Isosorbide dinitrate Sustained tx Prevent stable angina 20 - 45 min 2.5 - 6.5 mg 1 – 4 x daily 3 - 8 hrs Transdermal Nitroglycerine Sustained tx Prevent stable angina 20 – 60 min <ul><li>Patch 1 / day </li></ul><ul><li>Ointment </li></ul><ul><li>1-2 in., 4-6 hrs </li></ul><ul><li>Avoid tolerance </li></ul><ul><li>(PM respite) </li></ul>2 – 24 hrs
    142. 142. Nitroglycerin Patient/Family Education <ul><li>SL </li></ul><ul><ul><li>Tabs between cheek/lip & gum </li></ul></ul><ul><ul><li>Don’t swallow </li></ul></ul><ul><ul><li>1 tab q 5 min x 3, Call 911 if chest pain continues </li></ul></ul><ul><li>NO ALCOHOL! </li></ul><ul><li>Slow position changes; orthostatic hypotension </li></ul><ul><li>Headaches are not uncommon </li></ul><ul><li>Check expiration date on tablets </li></ul>
    143. 143. Angina Prophylaxis <ul><li>“ Medical management” of symptomatic coronary artery disease (stable angina) has been shown to have similar outcomes when compared with interventions such as balloon angioplasty with stenting. </li></ul><ul><li>Most stents are actually not FDA approved for stable angina. </li></ul><ul><ul><li>They are indicated for acute coronary syndromes (to be covered in a few minutes). </li></ul></ul>
    144. 144. Beta-adrenergic Blocking Agents <ul><li>Manage stable angina (not vasospastic) </li></ul><ul><li>Block beta-1 receptors </li></ul><ul><ul><li>Negative inotrope </li></ul></ul><ul><ul><li>Negative chronotrope </li></ul></ul><ul><ul><li>Negative dromotrope </li></ul></ul><ul><ul><li> reduce myocardial oxygen demand </li></ul></ul><ul><li>Prevent Sudden Death! </li></ul><ul><ul><li>More on these later…… </li></ul></ul>
    145. 145. Calcium Channel Blockers <ul><li>Verapamil, diltiazem, nifedipine </li></ul><ul><li>Manage stable & vasospastic angina </li></ul><ul><li>Block calcium entry into cell </li></ul><ul><ul><li>Arterial vasodilation </li></ul></ul><ul><ul><li>Decreases heart rate (SA node firing, AV node conduction) </li></ul></ul><ul><ul><li>Negative intotrope </li></ul></ul><ul><ul><li> reduce myocardial oxygen demand </li></ul></ul>
    146. 146. <ul><li>Anti-platelet drugs </li></ul><ul><li>Aspirin, </li></ul><ul><li>clopidorel (Plavix), </li></ul><ul><li>IIb,IIIa inhibitors (Repro) </li></ul><ul><li>Decrease platelet aggregation  </li></ul><ul><li>Prevent thrombus formation </li></ul><ul><li>Anticoagulants </li></ul><ul><li>Heparin, warfarin </li></ul><ul><li>Reduce fibrin production  </li></ul><ul><li>Suppress clotting </li></ul>OPEN! Keep arteries
    147. 147. Kumar (2003) IIb-IIIa Inhibitors Abciximab (RePro @ ) Alter Platelet Aggregation <ul><li>- Onset 2 hours </li></ul><ul><ul><li>- Duration 48 hours </li></ul></ul><ul><ul><li>- Infuse with filter </li></ul></ul>
    148. 148. Anti-platelet & Anticoagulant Drugs <ul><li>Contraindications </li></ul><ul><li>Active bleeding </li></ul><ul><li>CVA w/i 2 yrs </li></ul><ul><li>GI/GU bleeding </li></ul><ul><li>w/i 6 weeks </li></ul><ul><li>Thrombocytopenia </li></ul><ul><li>Aneurysm </li></ul><ul><li>Intracranial neoplasm </li></ul><ul><li>Major side effect BLEEDING </li></ul><ul><ul><li>Intracranial, retroperitoneal, hematemesis </li></ul></ul><ul><li>Labs </li></ul><ul><ul><li>PT/INR, PTT, Activated clotting Time (ACT), </li></ul></ul><ul><ul><li>platelet count </li></ul></ul>
    149. 149. You having an MI ??
    150. 150. Which of the following is present in stable angina? <ul><li>An unstable plaque. </li></ul><ul><li>A ruptured plaque </li></ul><ul><li>A stable plaque </li></ul><ul><li>A plaque with a thrombus. </li></ul>
    151. 151. Which of the following is diagnostic of an acute myocardial infarction? <ul><li>ST segment elevation </li></ul><ul><li>Increased serum CK-MB </li></ul><ul><li>Increased serum troponins </li></ul><ul><li>Increased C-reactive protein </li></ul>
    152. 152. Management of unstable angina or acute myocardial infarction must include interventions/medications that: <ul><li>Increase oxygen supply to the myocardium </li></ul><ul><li>Decrease the oxygen demands of the myocardium </li></ul><ul><li>Relieve the symptoms </li></ul><ul><li>All of the above </li></ul>
    153. 153. Need a break?
    154. 154. Heart Failure
    155. 155. Heart Failure <ul><li>Failure of the heart to function as a pump </li></ul><ul><li>Normally pumping ability adjusts to body needs for O 2 </li></ul><ul><li>Cardiac Reserve </li></ul><ul><ul><li>Ability to  CO during  need </li></ul></ul><ul><ul><li>Athletes have large cardiac reserve </li></ul></ul><ul><ul><li>HF pts (and elderly) have poor cardiac reserve </li></ul></ul>
    156. 156. Heart Failure <ul><li>HF involves interplay between 2 factors: </li></ul><ul><ul><li>Inability of failing heart to maintain sufficient CO to support body functions </li></ul></ul><ul><ul><li>Recruitment ( and subsequent failure) of compensatory mechanisms designed to maintain cardiac reserve </li></ul></ul>
    157. 157. Cardiac Output Stroke Volume Heart Rate Preload LVEDV Afterload SVR Contractility LVSWI Determinant of Cardiac Output
    158. 158. SV Contractility CO O 2 to Organs Trigger Compensatory Mechanisms Blood volume Vascular resistance Cardiac work HF
    159. 159. Vicious Cycle of Heart Failure Lehne, 2009, Pharmacology for Nursing Care, 7th ed., Elsevier, p. 518
    160. 160. Compensatory Mechanisms Maintain Vital Organ Perfusion <ul><li>Compensated heart failure </li></ul><ul><ul><li>Short term use </li></ul></ul><ul><li>Decompensated heart failure </li></ul><ul><ul><li>Compensatory mechanisms no longer effective </li></ul></ul><ul><ul><li>Compensatory mechanisms become detrimental </li></ul></ul>
    161. 161. Compensatory Mechanisms <ul><li>Frank Starling mechanism </li></ul><ul><li>Increased SNS activity </li></ul><ul><ul><li> HR,  preload d/t alpha receptor stimulation </li></ul></ul><ul><li>Renin-angiotensin-aldosterone system </li></ul><ul><li>Atrial natriuretic peptide </li></ul><ul><ul><li>Hormone release from atrial cells in response to  stretch. Promotes diuresis. </li></ul></ul><ul><li>Myocardial Hypertrophy </li></ul><ul><ul><li> in number of contractile elements in myocardial cells to  contractile performance </li></ul></ul>
    162. 162.
    163. 163.
    164. 164. Causes of CHF Impaired Cardiac Function Excess Work Demands Myocardial Disease Increased Pressure <ul><li>Cardiomyopathy </li></ul><ul><li>Systemic hypertension </li></ul><ul><li>Myocardial infarction </li></ul><ul><li>Pulmonary hypertension </li></ul><ul><li>Coronary artery disease </li></ul><ul><li>Coarctation of aorta </li></ul><ul><li>Myocarditits </li></ul>Increased Volume Work Cardiac Valve Disease <ul><li>A-V shunt </li></ul>Congenital Heart Defects <ul><li>Excessive administration of IV fluids </li></ul>
    165. 165. Heart Failure <ul><li>Pulmonary and/or systemic venous congestion </li></ul><ul><li>Described as </li></ul><ul><ul><li>Systolic vs diastolic failure </li></ul></ul><ul><ul><li>Right vs left sided failure </li></ul></ul>
    166. 166. Systolic vs Diastolic Failure <ul><li>Systolic dysfunction </li></ul><ul><ul><li>Impaired ejection of blood from heart during systole </li></ul></ul><ul><li>Diastolic dysfunction </li></ul><ul><ul><li>Impaired filling of ventricles during diastole </li></ul></ul><ul><li>Both elements may be present </li></ul><ul><ul><li>Most common form of heart failure, caused by myocardial ischemia or MI due to coronary atherosclerosis </li></ul></ul>
    167. 167. Systolic Dysfunction Impaired ejection  cardiac contractility   CO Conditions that  contractility: ischemic heart disease,  preload,  afterload Symptoms mainly result of  CO  “ forward” flow Porth 2005 28-4  EF
    168. 168. Diastolic Dysfunction Porth 2005 28-4 Impaired filling  LV Filling   CO Conditions that cause diastolic dysfunction: conditions that restrict diastolic filling - MV stenosis -  ventricular hypertrophy - Delay diastolic relaxation (aging)  EF
    169. 169. Right-sided vs Left-sided Failure Classified according to side of heart that is affected
    170. 170. “ Backward” “ Forward”
    171. 171. Right Heart Failure (RHF)  fluid accumulation in systemic venous system  venous congestion  peripheral edema Causes : Pulmonic valve stenosis or regurgitation RV infarction Cardiomyopathy PE (or anything else  PVR) Cor Pulmonale: RHF caused by lung disease Signs &Symptoms :
    172. 172. Left Heart Failure (LHF) Pathophysiology :  CO   LA & LV EDV & pulmonary pressure  eventually pulmonary edema. Causes : Acute MI Hypertension Cardiomyopathy MV stenosis/regurgitation Signs & Symptoms <ul><li>Renal dysfunction </li></ul>
    173. 173. BNP: B-Type natriuretic peptide <ul><li>Synthesized in myocardium of ventricles </li></ul><ul><li>Released in response to ventricular dilation & overload </li></ul><ul><li>Normal ~ 1-30 picogms/ml </li></ul><ul><ul><li>Normally increases with age, renal failure, </li></ul></ul><ul><ul><li>B-Blockers, diuretics </li></ul></ul>
    174. 174. BNP in Heart Failure <ul><li>Diagnosis </li></ul><ul><ul><li>BNP < 100, used to rule out new HF </li></ul></ul><ul><ul><li>Higher levels associated with more myocardial damage </li></ul></ul><ul><li>Prognosis and guiding therapy </li></ul><ul><ul><li>Increased risk of death or readmission, independent of clinical findings </li></ul></ul><ul><ul><li>Relevant changes in level and role for determining treatment </li></ul></ul>
    175. 175. HF Classifications ACC/AHA NYHA Functional Class A High Risk; no structural disease or symptoms B Structural disease; no symptoms I Asymptomatic C Structural disease with symptoms II Symptomatic w/ moderate exertion III Symptomatic w/ minimal exertion D Advanced structural disease; severe symptoms; invasive tx needed IV Symptomatic at rest
    176. 176. Heart Failure Management <ul><li>GOALS </li></ul><ul><li>1. Reduce myocardial restructuring / remodeling </li></ul><ul><ul><li>ACE-I, ARB, beta blockers </li></ul></ul><ul><li>2. Reduce/minimize symptoms </li></ul><ul><ul><li>improve quality of life!!! </li></ul></ul><ul><ul><li>diuretics, digoxin </li></ul></ul><ul><li>3. Improve contractility </li></ul><ul><ul><li>increase CO, vital organ perfusion </li></ul></ul><ul><ul><li>dobutamine, digoxin </li></ul></ul>
    177. 177. Diuretics Preload Vasodilators Afterload
    178. 178. Diuretic Therapy <ul><li>Furosemide (Lasix) </li></ul><ul><li>Ascending loop of Henle </li></ul><ul><li>Block Na+ & Cl- reabsorption  prevent water reabsorption </li></ul><ul><li>Rapid onset </li></ul><ul><ul><li>PO 60 min </li></ul></ul><ul><ul><li>IV 5 min </li></ul></ul>Lehne 2007, Fig 40-2
    179. 179. Loop Diuretics Adverse Effects <ul><li>Hypotension </li></ul><ul><ul><li>Volume loss </li></ul></ul><ul><ul><li>Venodilation </li></ul></ul><ul><li>Hypokalemia </li></ul><ul><ul><li>Ventricular dysrythmias </li></ul></ul><ul><ul><li>Increase risk of dig toxicity </li></ul></ul><ul><li>Hyponatremia </li></ul><ul><li>Hypochloremia </li></ul>
    180. 180. Afterload Reduction in HF  Vasodilation - Decrease resistance to ventricular ejection of blood - Improves forward blood flow - Reduce cardiac workload - Reduce compensatory myocardial remodeling
    181. 181. Angiotensin Converting Enzyme Inhibitors (ACE-I) <ul><li>(captopril, lisinopril, enalipril) </li></ul><ul><li>Mechanism of Action </li></ul><ul><li>Inhibit angiotensin I conversion to angiotensin II </li></ul><ul><li> Prevents vasoconstriction </li></ul><ul><li> Dilate arterioles (  afterload) </li></ul><ul><li> Decreases aldosterone release (  preload) </li></ul>
    182. 182. Angiotensin II Receptor Blockers (ARBs) <ul><li>(valsartan) </li></ul><ul><li>Mechanism of Action </li></ul><ul><li>Blocks actions of angiotensin II at its receptor </li></ul><ul><li>Aldosterone release Dilate arterioles </li></ul><ul><li>Na & H 2 O excretion </li></ul><ul><li>Afterload </li></ul><ul><li> Preload </li></ul>
    183. 183. ALL Heart Failure Patients SHOULD BE ON an ACE-I or ARB !!!!!!!! American College of Cardiologists, TJC, NQF, AHRQ
    184. 184. Beta blockers and HF <ul><li>Selective use due to negative inotropic effect </li></ul><ul><li>Decrease contractility and afterload  reduce cardiac re-modeling </li></ul><ul><li>Cardioselective beta blockers have been shown to improve morbidity & mortality </li></ul><ul><li>Ex. metoprolol ( beta) , bisoprolol ( beta) , carvedilol (alpha & beta blocker) </li></ul>
    185. 185. Digoxin: Considerations in HF <ul><li>Increases intracellular calcium concentration  improves contractility PLUS slows heart rate </li></ul><ul><li> Provides symptom relief </li></ul><ul><li>Treatment should begin with low doses (≤ 0.125 mg/d), esp. in elderly, women or kidney disease </li></ul><ul><li>Serum concentrations 0.5–0.9 ng/mL </li></ul><ul><li>Risk factors for digoxin toxicity (≥ 1 ng/mL): old age, female sex, high serum creatinine, use of non– potassium-sparing diuretics </li></ul><ul><li>ACE-I & ARBs Reduce digoxin therapeutic effect </li></ul>
    186. 186. <ul><li>Aldosterone receptor blocker (spironolactone [Aldactone]) </li></ul><ul><ul><li>Advanced HF, symptomatic despite ACE-I, dig, etc. </li></ul></ul><ul><ul><li>Blocks aldosterone receptors & actions </li></ul></ul><ul><ul><li>Benefits in HF </li></ul></ul><ul><ul><li> reduces cardiac remodeling </li></ul></ul><ul><ul><li> decreased sympathetic NS activation </li></ul></ul><ul><li>Positive inotropic agents: more on these later </li></ul>
    187. 187. The renin-angiotensin-aldosterone system contributes to worsening of heart failure and myocardial remodeling. Appropriate management includes administration of ______ which targets this system. <ul><li>Calcium channel blocker </li></ul><ul><li>Angiotensin converting enzyme inhibitor </li></ul><ul><li>Diuretic </li></ul><ul><li>Digoxin </li></ul>
    188. 188. A patient has severe mitral stenosis which greatly limits blood flow between the left atrium and the left ventricle. This condition may produce heart failure due to which of the following? <ul><li>Systolic dysfunction </li></ul><ul><li>Diastolic dysfunction </li></ul>
    189. 189. A patient is newly diagnosed with heart failure. Which of the following drugs should always be prescribed? <ul><li>A beta blocker </li></ul><ul><li>A calcium channel blocker </li></ul><ul><li>A diuretic </li></ul><ul><li>An ACE inhibitor or ARB </li></ul>
    190. 190. Need a break?? Can’t make it any longer….
    191. 191. Disorders of Heart Valves
    192. 192. Valvular Heart Disease <ul><li>Function of the valves is to ensure unidirectional flow of blood in the heart </li></ul><ul><li>Dysfunction of valves  </li></ul><ul><ul><ul><li>Narrowing of valve opening </li></ul></ul></ul><ul><ul><ul><li> does not open properly = Stenosis </li></ul></ul></ul><ul><ul><ul><li>Distortion of the valve </li></ul></ul></ul><ul><ul><ul><li> does not close properly = Regurgitation </li></ul></ul></ul>
    193. 193. Stenosis <ul><li>Valve does not open properly </li></ul><ul><li> resistance to blood flow thru valve </li></ul><ul><li> volume & work of the chamber that empties thru narrowed valve </li></ul><ul><ul><li>Ex. LA for mitral stenosis </li></ul></ul><ul><li>Produces distention in one chamber & impaired filling in another </li></ul>
    194. 194. Regurgitation <ul><li>Valve does not close properly </li></ul><ul><li>Permits backflow to occur when valve should be closed </li></ul><ul><ul><li>Ex. Blood flows back into LV during diastole when aortic valve should be closed </li></ul></ul><ul><li>Produces distention &  work demands on ejecting chamber </li></ul>
    195. 195. Mitral Valve Prolapse <ul><li>2-7% of the population </li></ul><ul><li>Most asymptomatic </li></ul><ul><li>Usually unknown cause, although can be associated with a variety of conditions </li></ul><ul><li>Palpations (awareness of the heartbeat) and dysrhythmias are common. </li></ul><ul><ul><li>Dysrhythmias may produce light-headedness or fainting. </li></ul></ul><ul><ul><li>Mitral regurgitation may necessitate valve repair or replacement. </li></ul></ul><ul><ul><li>Sudden death is rare. </li></ul></ul>Porth, 2007, Essentials of Pathophysiology, 2 nd ed., Lippincott, p. 407.
    196. 196. Valvular Heart Disease <ul><li>Valve defects are characterized by heart murmurs resulting from turbulent flow thru valve </li></ul><ul><li>Dysfunction d/t </li></ul><ul><ul><li>Congenital, trauma, ischemia, age, inflammation </li></ul></ul><ul><ul><li>Any valve can be involved </li></ul></ul><ul><ul><li>Aortic & mitral most common </li></ul></ul>
    197. 197. Diagram in Handout- Use it to figure out murmurs & Problems with blood flow d/t valvular defects!
    198. 198. Mitral Stenosis <ul><li>Incomplete opening of MV during diastole </li></ul><ul><ul><li> LA distention </li></ul></ul><ul><li>& impaired LV filling </li></ul><ul><li>Resistance thru MV  </li></ul><ul><li> LA dilates   LA pressures </li></ul><ul><li> pulmonary vasculature </li></ul><ul><li> pulmonary congestion & HTN </li></ul><ul><li>Symptoms of  CO occur with exertion, or  HR (  diastolic filling time) </li></ul>
    199. 199. Mitral Stenosis: Signs & Symptoms When would you hear a murmur? DIASTOLE
    200. 200. Mitral Valve Regurgitation <ul><li>Incomplete closure of MV </li></ul><ul><li>During systole, part of LV SV goes forward into aorta & regurgitant blood flows back into LA </li></ul><ul><li>Result  CO &/or pulmonary congestion </li></ul><ul><li>LV enlarges d/t  LVEDV </li></ul><ul><li>LA dilates d/t extra volume </li></ul><ul><li>Murmur heard during ???? </li></ul>
    201. 201. Mitral Valve Regurgitation <ul><li>Acute </li></ul><ul><ul><li> forward SV,  regurgitant SV </li></ul></ul><ul><ul><li>  LAP  pulmonary edema </li></ul></ul><ul><ul><li>Occur with MI, infective endocarditis </li></ul></ul><ul><li>Chronic </li></ul><ul><ul><li>Well tolerated, asymptomatic, until LV function becomes impaired </li></ul></ul><ul><ul><li>  forward SV,  regurgitant SV </li></ul></ul><ul><ul><li>  LAP  pulmonary edema </li></ul></ul>
    202. 202. Mitral Valve Regurgitation <ul><li>Management </li></ul><ul><li>Acute </li></ul><ul><ul><li>Improve forward flow with vasodilator, eg nitroprusside </li></ul></ul><ul><ul><li>MV repair, reconstruction, replacement </li></ul></ul><ul><li>Chronic </li></ul><ul><ul><li>MV repair, reconstruction, replacement </li></ul></ul>
    203. 203. Aortic Valve Stenosis <ul><li> resistance to ejection of blood from LV into aorta </li></ul><ul><li> resistance   work of LV &  volume of blood ejected into systemic circulation </li></ul><ul><li>Manifestations </li></ul><ul><ul><li>R/T  SV </li></ul></ul><ul><ul><li>Hypotension, syncope, angina, fatigue,  HR (takes longer to eject volume) </li></ul></ul>
    204. 204. Aortic Valve Regurgitation <ul><li>Incompetent AoV </li></ul><ul><li> backflow of blood to LV during diastole </li></ul><ul><li>  LV volume d/t LA & blood leaking back thru incompetent valve </li></ul><ul><li>Turbulent flow across AV during diastole  high pitched blowing sound </li></ul>
    205. 205. Aortic Valve Regurgitation <ul><li>Acute </li></ul><ul><ul><li>Sudden uncompensated  LVEDP  pulmonary edema &  CO  sympathetic stimulation  </li></ul></ul><ul><ul><li>peripheral vasoconstriction  </li></ul></ul><ul><ul><li> afterload   CO </li></ul></ul><ul><li>Chronic </li></ul><ul><ul><li>Compensated for a while </li></ul></ul>
    206. 206. Valve Disease Summary
    207. 207. Which of the following might produce pulmonary edema? <ul><li>Mitral stenosis </li></ul><ul><li>Pulmonic stenosis </li></ul><ul><li>Tricuspid stenosis </li></ul><ul><li>Tricuspid regurgitation </li></ul>
    208. 208. Kathryn !!! Pleeeaaase! Release the students! Mmmm…excellent!
    209. 209. Shock: The rude unhinging of the machinery of life!
    210. 210. Shock <ul><li>Adequate perfusion of body tissues depends on: </li></ul><ul><ul><li>Functioning heart to pump 0 2 into systemic circulation </li></ul></ul><ul><ul><li>A vascular system to transport O 2 to tissues </li></ul></ul><ul><ul><li>Sufficient amount of blood/O 2 </li></ul></ul><ul><ul><li>Tissues able to extract O 2 , nutrients from blood </li></ul></ul><ul><li>Shock is a condition in which </li></ul><ul><li>O 2 & energy supply to tissues is not adequate to meet demands </li></ul>
    211. 211. Shock Impairment of cellular metabolism <ul><li>Impairment of oxygen use </li></ul><ul><ul><li>Aerobic to anaerobic metabolism </li></ul></ul><ul><li>Impairment of glucose use </li></ul><ul><ul><li>Impaired glucose delivery or impaired glucose uptake </li></ul></ul>
    212. 212. Global Tissue Oxygenation Made Ridiculously Simple SvO2 = 75% 25% Venous Oxygen Delivery Arterial Oxygen Delivery Oxygen Consumption 100%
    213. 213. Aerobic Metabolism Anaerobic Metabolism 36 molecules ATP 2 molecules ATP Supports normal cell function Eventual cell dysfunction
    214. 214. 4 Types of Circulatory Shock <ul><li>Hypovolemic </li></ul><ul><ul><li>Diminished blood volume  inadequate filling of vascular compartment </li></ul></ul><ul><ul><ul><li>Loss of whole blood/plasma, extracellular fluid </li></ul></ul></ul><ul><li>Cardiogenic </li></ul><ul><ul><li>Failure of the heart to function as a pump </li></ul></ul><ul><li>Obstructive </li></ul><ul><ul><li>Mechanical barrier to blood flow in circulation </li></ul></ul><ul><ul><ul><li>PE, cardiac tamponade </li></ul></ul></ul><ul><li>Distributive </li></ul><ul><ul><li>Enlargement of vascular compartment </li></ul></ul>
    215. 215. Compensatory Mechanisms <ul><li>Sympathetic Nervous System </li></ul><ul><li> Heart rate </li></ul><ul><li> Respiratory rate </li></ul><ul><li> Glycolysis </li></ul><ul><li> Urine output </li></ul><ul><li> Blood flow to internal organs </li></ul><ul><li> Peristalsis </li></ul><ul><li>Cool skin </li></ul><ul><li>Diaphoresis </li></ul>
    216. 216.
    217. 217.
    218. 218. Cardiogenic Shock
    219. 219. Preload SV Restore Cardiac Pump  Ventricular Contractility Positive Inotropic Agents Depressed Normal Enhanced
    220. 220. Enhance Contractility <ul><li>Beta –1 Effect, increase contractility </li></ul><ul><li>Epinephrine </li></ul><ul><li>Dobutamine </li></ul><ul><li>Dopamine </li></ul><ul><li>Administration </li></ul><ul><li>Correct hypovolemia 1 st !! </li></ul><ul><li>Use infusion pump </li></ul><ul><li>Central venous catheter (CVC) preferred route </li></ul>
    221. 221. Dobutamine <ul><li>Beta-1 selective adrenergic agonist </li></ul><ul><li>First line to increase cardiac output </li></ul><ul><ul><li>Increase contractility & HR via beta-1 </li></ul></ul><ul><ul><li>Typical dose 2.5 – 10 microgm/kg/min </li></ul></ul><ul><li>Adverse Effects </li></ul><ul><ul><li>Dysrhythmias </li></ul></ul><ul><ul><li>When possible give via central venous catheter (CVC) !! </li></ul></ul>
    222. 222. Epinephrine <ul><li>Non-selective adrenergic agonist </li></ul><ul><li>First line in cardiac arrest & anaphylaxis </li></ul><ul><ul><li>Increase contractility & HR via beta-1 </li></ul></ul><ul><ul><li>Vasoconstriction via alpha-1 </li></ul></ul><ul><ul><li>Bronchodilation via beta-2 </li></ul></ul><ul><li>Adverse Effects </li></ul><ul><ul><li>Dysrhythmias </li></ul></ul><ul><ul><li>Angina </li></ul></ul><ul><ul><li>Hyperglycemia in diabetics </li></ul></ul><ul><ul><li>Necrosis w/ extravasation </li></ul></ul><ul><ul><li>Give via CVC!! </li></ul></ul>
    223. 223. Epinephrine <ul><ul><li>Cardiac Arrest </li></ul></ul><ul><ul><li>IV Push </li></ul></ul><ul><ul><ul><li>Pre-filled syringe </li></ul></ul></ul><ul><ul><li>Intracardiac </li></ul></ul><ul><ul><ul><li>Pre-filled syringe </li></ul></ul></ul><ul><ul><ul><li>w/ really long needle! </li></ul></ul></ul><ul><ul><li>IV infusion </li></ul></ul><ul><ul><li>Increase contractility </li></ul></ul>
    224. 224. Cardiogenic Shock Vasodilators Afterload
    225. 225. Afterload Manipulation: Restore perfusion or Decrease Work of Heart <ul><li> Systemic Vascular Resistance (SVR) </li></ul><ul><li>Vasopressors   SV & CO </li></ul><ul><li> BP & perfusion pressure </li></ul><ul><li> SVR </li></ul><ul><li>Vasodilators   SV& CO </li></ul><ul><li> BP & work of heart </li></ul>SV SVR
    226. 226. Sodium Nitroprusside (Nipride) <ul><li>Arterial vasodilator </li></ul><ul><li>reduces resistance to LV ejection </li></ul><ul><li>Improves forward flow & increases SV </li></ul><ul><li>reduces “backward” pressure in the pulmonary vasculature </li></ul><ul><li>decrease pulmonary congestion </li></ul><ul><li>Also used in acute mitral regurgitation & hypertensive emergencies </li></ul>
    227. 227. Hypovolemic Shock <ul><li>Acute loss of 15-20% of blood volume </li></ul><ul><li>Characterized by  blood volume  inadequate filling of the vascular compartment </li></ul><ul><ul><li> venous return to right heart </li></ul></ul><ul><ul><li> preload </li></ul></ul><ul><ul><li> SV   CO </li></ul></ul><ul><ul><li> 02 delivery to tissues </li></ul></ul>
    228. 228. Hypovolemic Shock
    229. 229. Clinical Manifestations <ul><li>Mild </li></ul><ul><ul><li> HR,  BP, cool extremities </li></ul></ul><ul><li>Moderate </li></ul><ul><ul><li>HR >100, sBP~90, Restless, diaphoretic, oliguria </li></ul></ul><ul><li>Severe </li></ul><ul><ul><li>HR >120, BP<60, cold extremities,  LOC </li></ul></ul>
    230. 230. Frank-Starling Curve: Preload SV LVEDV LV dysfunction Hypovolemia Normal
    231. 231. Restore Intravascular Volume <ul><li>Crystalloid Infusion Isotonic Fluids </li></ul><ul><li>0.9% NaCl </li></ul><ul><ul><li>(“Normal Saline”) </li></ul></ul><ul><li>Plasmalyte (pH 7.40) </li></ul><ul><li>Ringers Lactate </li></ul><ul><li>Colloid Infusion “Volume Expander” </li></ul><ul><li>Albumin </li></ul><ul><li>Hetastarch (Hespan) </li></ul>
    232. 232. Stop Intravascular Volume Loss &/or DIC <ul><li>Blood products </li></ul><ul><ul><li>Platelets  plug the holes </li></ul></ul><ul><ul><li>Fresh frozen plasma ( FFP)  correct coags </li></ul></ul>Restore Oxygen Carrying Capacity <ul><ul><li>PRBC  replace lost boxcars </li></ul></ul><ul><ul><li>Erythropoietin </li></ul></ul>
    233. 233. Distributive S hock <ul><ul><li>Loss of vessel tone, enlargement of vascular compartment, displacement of vascular volume away from heart & central circulation </li></ul></ul><ul><ul><li>Loss of sympathetic tone ( neurogenic SCI ) </li></ul></ul><ul><ul><li>Presence of vasodilating substances in blood ( anaphylactic shock ) </li></ul></ul><ul><ul><li>Presence of inflammatory mediators in blood ( septic shock ) </li></ul></ul>
    234. 234. Septic Shock <ul><li>Associated with severe infection and the systemic response to the infection. </li></ul><ul><li>Gram negative organisms most common </li></ul><ul><li>Mechanisms related to mediators of inflammatory response  </li></ul><ul><ul><li>Vasodilation </li></ul></ul><ul><ul><li> capillary permeability </li></ul></ul><ul><li>Endotoxins induce tissue damage by activating coagulation cascade </li></ul><ul><li>Manifests as fever, vasodilation </li></ul>
    235. 235.
    236. 236. Septic shock <ul><li>Endotoxin & inflammatory mediator release  </li></ul><ul><li>Vasodilation  Decrease preload </li></ul><ul><li>  Increase cardiac output </li></ul><ul><li>Capillary “leakage”  Edema </li></ul><ul><li>Coagulopathies  Disseminated Intravascular Coagulation (DIC) </li></ul>
    237. 237. What is SIRS? Systemic Inflammatory Response Syndrome Often a precursor to sepsis! <ul><li>Clinical response arising from a nonspecific insult. </li></ul><ul><li>SIRS criteria includes 2 or more of the following: </li></ul><ul><ul><li>Temperature > 38  C or < 36  C </li></ul></ul><ul><ul><li>Heart Rate > 90 beats/min </li></ul></ul><ul><ul><li>Respiration > 20 breaths/min </li></ul></ul><ul><ul><li>WBC > 12,000/mm 3 , < 4,000/mm 3 or >10% immature cells (bands) </li></ul></ul><ul><ul><li>PaCO 2 < 32mm Hg </li></ul></ul>
    238. 238. Continuum of S epsis SIRS with a suspected or confirmed infx Sepsis SIRS Septic Shock ≥ 2 of the following: Temp: >38°C or < 36 °C H R: >90 beats/min Resps: >20/min WBC : >12,000/mm 3 , or < 4,000/mm 3 1992 Consensus Conf Bone et al. Chest. 1992;101:1644-1654. ; 2001 SCCM/ESICM/ACCP/TS/SIS International Sepsis Definition Conference. Crit Care Med 2003 31(4):1250-1256. Sepsis + Hypotension despite fluid + perfusion abnormalities + MODS (>1 organ failure, inability to maintain homeostasis w/o tx) Severe Sepsis Sepsis + > 1 organ dysfunction
    239. 239. Sepsis Resuscitation Bundle within 1 st hour of recognition <ul><li>Obtain serum lactate </li></ul><ul><li>Blood cultures (percutaneous) prior to antibiotics </li></ul><ul><li>Antibiotics </li></ul><ul><li>Initiate BP, CVP & ScvO2 monitoring </li></ul><ul><li>If CVP < 8 mmHg, Hypotension &/or Lactate >4 </li></ul><ul><li>Start: </li></ul><ul><li>1000ml crystalloid over 30 min. </li></ul><ul><li>Vasopressor if no response to fluid </li></ul><ul><li>(Clinically important but not on exam) </li></ul>Dellinger P, et al: Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock 2008. Crit Care Med . 2008;36(1):296-327
    240. 240. Sepsis Resuscitation Bundle within 1 st 6 hours of recognition <ul><li>PRBC for Hgb < 7 g/dl, target 7-9 g/dl </li></ul><ul><li>Fluid to keep CVP > 8 mmHg </li></ul><ul><li>MAP > 65 mmHg </li></ul><ul><ul><li>Crystalloid; Vasopressor if no response to fluid </li></ul></ul><ul><li>ScvO2 > 70 % </li></ul><ul><ul><li>Dobutamine; RBC if Hct < 30% </li></ul></ul><ul><li>Transfer to ICU </li></ul><ul><li>(Clinically important but not on exam) </li></ul>Dellinger P, et al: Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock 2008. Crit Care Med . 2008;36(1):296-327
    241. 241. Catecholamines: Adrenergic Agonists Alpha 1 Beta 1 Beta 2 Dopamine Vasoconstrict Cardiac stimulation Bronchodilate Renal artery dilation Phenylephrine Epinephrine Norepinephrine (Levophed) Dobutamine Dopamine Dopamine Dopamine
    242. 242. Complications of Shock <ul><li>“ Shock not only stops the machinery, but it wrecks the machinery” (Wiggers) </li></ul><ul><li>Many body systems are “wrecked” by shock </li></ul><ul><li>Complications </li></ul><ul><ul><li>Acute respiratory failure/respiratory distress syndrome </li></ul></ul><ul><ul><li>Acute renal failure </li></ul></ul><ul><ul><li>GI bleeding </li></ul></ul><ul><ul><li>Disseminated intravascular coagulation </li></ul></ul><ul><ul><li>Multiple organ dysfunction syndrome </li></ul></ul>
    243. 243. Cardiac Output Stroke Volume Heart Rate Preload Afterload Contractility Management of Shock: Oxygen Delivery SaO2 & Hgb X Reverse the causative factor(s) Restore perfusion to cells, tissues, organs
    244. 244. Global Tissue Oxygenation Made Ridiculously Simple SvO2 = 75% 25% Venous Oxygen Delivery Arterial Oxygen Delivery Oxygen Consumption 100%
    245. 245. Appropriate treatment of hypotension related to cardiogenic shock includes: <ul><li>Volume infusion </li></ul><ul><li>Vasopressor (eg levophed) </li></ul><ul><li>Positive inotrope (eg dobutamine) </li></ul><ul><li>Increasing heart rate (eg atropine) </li></ul>
    246. 246. Appropriate treatment of hypotension related to hypovolemic shock includes: <ul><li>Volume infusion </li></ul><ul><li>Vasopressor (eg levophed) </li></ul><ul><li>Positive inotrope (eg dobutamine) </li></ul><ul><li>Increasing heart rate (eg atropine) </li></ul>
    247. 247. Which of the following will produce cold extremities? <ul><li>Cardiogenic shock </li></ul><ul><li>Anaphylactic shock </li></ul><ul><li>Septic shock </li></ul><ul><li>Spinal shock </li></ul>
    248. 248. SaO 2 /Hb CO O 2 Utilization Extraction & VO 2 Venous Return SvO 2 O 2 Delivery
    249. 249. Questions?

    ×