March Cardio Review


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The power point of the CC Cardiology review from LNSC March 2013.

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  • Think of the EKG tracings for Lead I and III as someone looking at you, holding out their thumbs with their right thumb as Lead I and their left thumb as Lead III.
  • Lead I (Right) is upright. Lead III (left) is upright.
  • Lead I (Right) is upright. Lead III (left) is down. Consult Lead II, if it is also down, then it is an anterior hemiblock.
  • Lead I (Right) is down. Lead III (left) is up. Most likely a posterior hemiblock.
  • Lead I (Right) is down. Lead III (left) is down. This indicates a possible bifasicular block.
  • Keep the rate up, may give Dobutamine
  • March Cardio Review

    1. 1. Cardiac ReviewA&P, EKG, MI, Other Cardiac Emergencies
    2. 2. What is ACS?• ACS is coronary disease that is causing an acute illness, inclusive of: – Ischemia/unstable angina (UA or USA) – Non-ST Elevation MI (NSTEMI) – ST Elevation MI (STEMI)• STEMI and NSTEMI are relatively new terms; “NQMI” and similar terms are no longer used• The term “AMI” is still used and is usually synonymous with STEMI
    3. 3. Epidemiology of ACS• AMI most common 6am to noon due to elevated bp, catacholamines and platelet aggregability• AMI more common in winter• >1 million infarcts/500k US deaths per year• Leading cause of mortality in US• Annual cost >$120 billion per year
    4. 4. STEMI• Acute phase is <6 hrs from onset• Immediate transfer to interventional cardiac cath lab is most effective treatment!• Fibrinolytics is also definitive treatment
    5. 5. Anatomy, PathoPhysiology
    6. 6. Cardiac A&P
    7. 7. Layers of the Heart• 1. Endocardium-inner• 2. Myocardium- middle• 3. Epicardium-outer• 4. Pericardium-sac around heart
    8. 8. Blood Flow through Heart • Blood flows from VC to the R atria. • It crosses the tricuspid valve into the R ventricle. • It goes past the pulmonic valve into the pulmonary artery and the lungs.
    9. 9. Blood Flow cont. • Blood comes from the lungs via the pulm. veins into the L atria. • It crosses the mitral valve into the L vent. • It goes past the aortic valve into the aorta and the systemic and coronary circulation.
    10. 10. Heart Valves **Valve order T-P-M-A**• Two types: atrioventricular and semilunar.• AV: Open as the result of lower ventricular pressure – Tricuspid and Mitral valves• Semilunar: Located between the ventricles and great arteries – Pulmonic and Aortic
    11. 11. Coronary Circulation• Right and Left coronary arteries originating at the coronary ostia at the base of the aorta. – Left Coronary Artery • Left Anterior Descending – Anterior, 2/3 of the septum, partial lateral wall • Left Circumflex – Primary Lateral Wall circulation – Right Coronary Artery • Right atrium, right ventricle, inferior & posterior wall of left ventricle.
    12. 12. Anterior Coronary Circulation
    13. 13. Posterior Coronary Circulation
    14. 14. Properties of Cardiac Cells• Automaticity• Excitability• Conductivity• Contractility
    15. 15. • Polarization: No electrical activity. Inside of cell negative.• Depolarization: Na+ rapidly rushes in and causes inside to become positive.• Repolarization: Na+ stops and K+ leaks out as cell returns to resting levels.
    16. 16. Conduction System
    17. 17. Conduction System in Action
    18. 18. SA Node • Initiates electrical impulses at a rate of 60- 100 bpm. • Reaches threshold and depolarizes more rapidly than other cardiac cell. • Blood supply from SA node artery (from RCA in 55% of hearts).
    19. 19. Internodal Pathways • Anterior • Middle • Posterior
    20. 20. Atrioventricular Junction • AV node and Bundle of His • Electrical link between atria and ventricle
    21. 21. AV Node• Supplied by RCA in 90% of hearts and LCx in 10%.• Delays conduction to allow atria to empty
    22. 22. Bundle of His• Dual blood supply from LAD and PDA• Intrinsic pacemaker rate of 40-60 bpm• Normally is the only electrical connection between the atria and the ventricles.
    23. 23. Right and Left Bundle Branch • RBB innervates RV • LBB innervates the septum and LV • LBB has 3 divisions: – Anterior fascicle – Posterior fascicle – Septal fascicle
    24. 24. Purkinje Fibers• Spread from the septum into the papillary muscles and downward into the apex of the heart• Penetrates 1/3 of the way into the ventricle muscle mass• Intrinsic rate of 20-40 bpm
    25. 25. Electrophysiology• Depolarization – Complete depolarization normally results in muscle contraction• Threshold – minimal stimulus required to produce excitation of myocardial cells
    26. 26. Electrophysiology• Repolarization – Process of returning to resting potential state • Sodium influx stops and potassium leaves cell • Sodium pumped to outside the cell – Relative refractory period • cell will respond to a second action potential but the action potential must be stronger than usual – Absolute refractory period • cell will not respond to a repeated action potential regardless of how strong it is
    27. 27. Electrophysiology Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ K+ K+ K+ K+ K+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+Myocardial cells are POLARIZED. They have more positive chargesoutside than inside.
    28. 28. Electrophysiology Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ K+ K+ K+ K+ K+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+ Na+Stimulation of cell opens “fast” channels in cell membrane. Na+ rapidlyenters cell. Now there are more positive charges inside than outside.The cell is DEPOLARIZED.
    29. 29. Electrophysiology• Depolarization causes Ca2+ to be released from storage sites in cell.• Ca2+ release causes contraction. Calcium couples the electrical event of depolarization to the mechanical event of
    30. 30. Electrophysiology Na+ Na+ Na+ Na+ K+ Na+ Na+ Na+ Na+ Na+ K+ K+ Na+ Na+ K+ Na+ Na+ Na+ Na+ Na+ K+ Na+ Na+Cell then REPOLARIZES by pumping out K+ then Na+ to restorenormal charge balance.
    31. 31. Electrophysiology Na+ Na+ Na+ Na+ K+ Na+ Na+ Na+ Na+ Na+ K+ K+ Na+ Na+ K+ Na+ Na+ Na+ Na+ Na+ K+ Na+ Na+Finally, the Na+-K+ pump in the cell membrane restores the properbalance of sodium and potassiuim.
    32. 32. Cardiac Conduction CyclePhase 0 = rapid Na influxPhase 1 = stop Na influx, K efflux, Cl influxPhase 2 = Ca influx, K influx Sarcomere:Phase 3 = stop Ca influx, minimal K efflux, Na Fast Sodiumefflux ChannelsPhase 4 = resting membrane potential state
    33. 33. EKG Basics
    34. 34. What is an electrocardiogram?• Picture of the electrical activity of the heart• Used to evaluate/monitor heart rate, effects of disease, meds, or injury, pacemaker function, electrolytes, conduction disturbances, mass of muscle, orientation of heart in chest or presence of ischemic damage.
    35. 35. Leads• Record of electrical activity between two electrodes.• Averages the current flow at a specific time in a portion of the heart.• 3 types: standard limb leads, augmented leads and precordial (chest) leads.• Each has positive and negative pole.• The positive electrode is like an “eye”.
    36. 36. Leads (cont.)• If the impulse is moving toward the positive electrode the waveform goes up.• If away, the waveform goes down.• If perpendicular, it will either be biphasic or a straight line.• No electrical activity is called the baseline or isoelectric line.
    37. 37. Standard Limb Leads• Leads I, II, III• Einthoven’s triangle• The voltage of I + III = II
    38. 38. Lead I • Shows lateral surface of the left ventricle • Normally is upright because the impulse is moving toward the positive electrode.
    39. 39. Lead II • Views inferior surface of the left ventricle • Normally positive • Commonly used for monitoring
    40. 40. Lead III • Views inferior surface of the left ventricle • Usually the QRS is positive but the P may be +, - or biphasic
    41. 41. Augmented Limb Leads• Letters stand for “augmented voltage ___”• Only consist of one electrode on the body surface• Negative point is the center
    42. 42. aVR • Views heart from right shoulder • Does not view the walls of the heart, only the base and great vessels • Normally negative
    43. 43. aVL • Views heart from the left shoulder • Views high lateral wall of the left ventricle • Usually biphasic because depolarization is perpendicular to the electrode
    44. 44. aVF • Views the heart from the left leg • Views the inferior wall of the left ventricle • Should be positive
    45. 45. Precordial (Chest) Leads• View the heart in the horizontal plane• Each electrode is positive
    46. 46. V leads cont.• V1: 4th ics to right of sternum, septum, negative• V2: 4th ics to left of sternum, septum, biphasic• V3: midway between V2 & V4, anterior, biphasic• V4: 5th ics midclavicular line, anterior, biphasic• V5: between V4 & V6 @ 5th ics, lateral, positive• V6: midaxillary line in 5th ics, lateral, positive
    47. 47. Horizontal Plane (chest leads)
    48. 48. ECG Lead Placement
    49. 49. R wave progression• From V1 to V6 the direction of the QRS complex should change from negative to positive in a gradual manner
    50. 50. R Wave Progression
    51. 51. ECG paper
    52. 52. Waveforms
    53. 53. Waveforms and Intervals
    54. 54. 12 Lead Layout
    55. 55. 12 Lead EKG Technique• Effective contact between electrode and skin is essential• Try to exclude artifact – Internal (larger patients) – External (60hz noise)• Precise placement of precordial electrodes• Correct patient position
    56. 56. Technically Accurate EKG Tracing• Remember Einthoven’s triangle • Lead I + Lead III = Lead II • P waves positive in lead II and negative in aVR• R waves in V1-V6 should gradually progress from negative to upright• Check standardization box before interpreting the EKG tracing
    57. 57. Interpretation of the 12-Lead ECG• In the limb leads – P wave is typically upright in leads I, II, aVL and aVF – P wave is often biphasic in lead III and is negatively deflected in lead aVR• In precordial leads – P wave is typically upright in leads V5 and V6 – Lead V1 is biphasic, and leads V2 and V4 are variable
    58. 58. Interpretation of the 12-Lead ECG• Septal depolarization is not always seen on the ECG. When it is, there will be a small Q wave in leads I, aVL, V5, and V6.• The T wave will usually be recorded in a positive deflection in the same leads that record a positive deflection in the R wave.
    59. 59. Systematic Approaches• Use the same method of analysis each time to ensure consistent interpretation.• Questions to consider when looking for arrhythmias – Is the rhythm fast or slow? – Is the rhythm regular or irregular? – Are there any P waves? – Are all P waves the same?
    60. 60. Systematic Approaches• Questions to consider (continued) – Does each QRS complex have a P wave? – Is the PR interval constant? – Are the P waves and QRS complexes associated with each other? – Are the QRS complexes narrow or wide? – Are the QRS complexes grouped or not? – Are there any dropped beats?
    61. 61. Blocks and Axis Deviation
    62. 62. Hemiblock• Block of one of the two fascicles of the left bundle branch system• Marked axis deviation often indicates hemiblock
    63. 63. Trifascicular System• Part of the electrical conduction system – Right bundle branch – Left bundle branch • Branches into two separate fascicles • Left anterior hemifascicle (fascicle) • Left posterior hemifascicle (fascicle)
    64. 64. Remember This?
    65. 65. Trifascicular System• Electrical impulse can travel to the ventricles in three ways: – Right bundle branch – Left anterior hemifascicle • Blood supply from LAD – Left posterior hemifascicle – Blood supply from RCA and circumflex
    66. 66. Left Anterior Hemiblock• Anterior hemifascicle of left bundle branch blocked – Ischemia, necrosis• ECG finds: – Pathological left-axis deviation – Small Q wave in LI – Small R wave in LIII – Narrow QRS possible
    67. 67. Left Anterior HemiblockBledsoe/Benner, Critical Care Paramedic
    68. 68. Left Posterior Hemiblock• Posterior fascicle of left bundle branch blocked• ECG finds: – Pathological right-axis deviation – Small R waves in LI – Small Q waves in LIII – Right ventricular hypertrophy• Clinically more significant than left anterior block
    69. 69. Left Posterior Hemiblock
    70. 70. Clinical Significance of Hemiblock• Mortality rate for patients with AMIs with hemiblocks four times greater than those without• Risk factor for complete heart block – Patient considered high risk if AV block presents with hemiblock• In AMI setting, can indicate proximal artery occlusion
    71. 71. Axis• Definition: axis is the average vector (direction) of the cardiac electrical impulse in the vertical plane.• We are concerned with the QRS axis, which is the direction of the ventricular depolarization impulse.
    72. 72. Axis• What does this mean? – The electrical impulse that depolarizes the heart travels a certain route thru the heart – The vertical plane is the one that runs head to toe when the patient is facing forward – The average direction the impulse travels in this plane is the axis – Simple, right?!
    73. 73. Axis• Measured in degrees – 0° is at 3 o’clock – 180° is at 9 o’clock – Degrees are positive from 3 o’clock to 9 o’clock in clockwise direction – Degrees are negative from 3 o’clock to 9 o’clock in counterclockwise direction
    74. 74. Axis Quadrants• The axis circle is divided into four quadrants – Normal= 0° to +90° – RAD= +90° to ±180° – LAD= 0° to -90° – Indeterminate axis= -90° to ±180°• This makes sense as the normal impulse travels from SA node to ventricles in a SW direction!• All quadrants besides normal are “deviated”
    75. 75. Rapid Axis and Hemiblock Determination• See “Rapid Axis and Hemiblock Chart” on the next slide. – Designed to help clinicians quickly determine presence of axis deviation and hemiblock• Two ways to use chart – When cardiac monitor does not provide axis angle: • Assess LI, II, and III on ECG • Determine if QRS complex is deflected more positively or negatively in each lead • Compare finds to “Rapid Axis and Hemiblock Chart” – When cardiac monistor provides axis angle: • Compare monitor readout (don’t trust machine)
    76. 76. Rapid Axis andHemiblock Determination
    77. 77. Thumbs Up/Down Hemiblock• Useful for quick determination• Lead I and III – visualize as thumbs of someone facing you
    78. 78. Normal Axis
    79. 79. Left Deviation
    80. 80. Right DeviationBledsoe/Benner, Critical Care Paramedic
    81. 81. Extreme Right Deviation
    82. 82. Significance of Axis Deviation• Shifts away from infarcted tissue• Left Deviation – Left Hypertrophy, WPW, Septal defects, Hyperkalemia• Right Deviation – Right Hypertrophy, Left Posterior Hemiblock, PE, Atrial defects, Chronic lung disease• Extreme Right – V-Tach, Paced, Anterolateral Infarct
    83. 83. Bundle Branch Blocks• Definition – Block to the left or right bundle branch system • Left bundle branch block more clinically significant – Higher mortality – Results in wide QRS ∀ >120 ms• Etiology – Myocardial ischemia, infarction – Congenital defects
    84. 84. Bundle Branch Blocks
    85. 85. Bundle Branch Blocks
    86. 86. Bundle Branch Blocks “Turn Signal Criteria”• MCL-1, any of the precordial leads can be used• QRS must be >120 ms
    87. 87. Bundle Branch Blocks “Turn Signal Criteria”• Technique • View the QRS of V1 (or MCL-1) • Lies immediately over the right ventricle and provides the best view of the superior aspect of the interventricular septum • Identify the J point of the QRS • Draw a horizontal line from the J point either to an intersecting line of the QRS or to the beginning of the QRS • Will produce a triangle pointing upward or downward • When pointing upward, triangle indicates a right bundle branch block • When you push a vehicle’s turn signal upward, the signal lights indicate a right turn • When pointing downward, triangle indicates left bundle branch block • When you pull a vehicle’s turn signal downward, the signal lights indicate a left turn
    88. 88. Bundle Branch Blocks “Turn Signal Criteria”
    89. 89. Rate-Dependent Bundle Branch Blocks• Bundle blocks appreciated with tachycardic rhythms – A-fib – A-flutter• Tachycardia results in: – Increased myocardial oxygen demand – Decreased preload • Decreased preload = decreased cardiac output – Decreased cardiac output can lead to ischemia
    90. 90. Rate-Dependent Bundle Branch Blocks• Easy to misidentify as VT – VT therapy could result in rapid hemodynamic compromise• MCL-1 useful for differentiating tachycardia with BBB from VT – RSR’ complex >120 ms = RBBB, not VT – QRS >120 ms = LBBB, not VT
    91. 91. Chest Pain and MI
    92. 92. Coronary Plaques• Have the consistency of toothpaste• Cells within plaque synthesize and secrete proteins that promote clot formation• Prone to rupture if they are large and have a soft lipid core
    93. 93. Coronary Artery Obstruction• If the clot partially occludes the artery: – Acute coronary syndrome or unstable angina• If the clot fully occludes the artery: – Myocardial infarction
    94. 94. Angina• Stable – Onset with physical exertion or stress. Lasts 1 – 5 minutes and is relieved by stress.• Unstable – Change in Stable angina frequency, quality, duration, or intensity. Lasts >10 minutes despite rest and/or NTG.• Variable – Spontaneous noted at rest (sleeping); relieved by NTG• Silent – Asymptomatic with evidence of ischemia• Mixed – Combination of the above
    95. 95. Types of Infarctions• Divided into Transmural and non-transmural MIs.• Transmural: Extends through full thickness of the myocardium and includes the endocardium and epicardium.• Subendocardial: Damage is limited to the subendocardial surface.
    96. 96. Ischemia, Injury and Infarction – 12 Leads• Changes usually begin early and progress• May take more than an hour for changes to show• 20-30% of infarcts do not change the 12-lead EKG -must base diagnosis on labs and clinical presentation
    97. 97. Hyperacute T Waves• The T wave can become tall and narrow because of ischemia.• The first change that might appear is an upward slanting of the ST segment and a subtle enlargement of the T wave.• The hyperacute T waves are localized to the area of ischemia and infarction.
    98. 98. ST-Segment Elevation• Caused by changes that affect ventricular depolarization and repolarization• Non-MI changes can also cause this condition – Left BBB – Ventricular rhythms – LVH – Pericarditis – Early repolarization
    99. 99. ST-Segment Elevation• A persistent ST-segment elevation may indicate a ventricular aneurysm.• In benign J-point elevation, the T wave is clearly distinguished as a separate wave.• With myocardial disease, the elevated J point bows upward and merges with the T wave.
    100. 100. J-PointPoint where QRS ends and ST segment begins
    101. 101. Sharp and Diffuse J Points
    102. 102. Ischemia• Lack of blood may be due to a decreased supply or an increased demand – Causes a delay in repolarization• ST segment is depressed if it is more than 1 mm below the isoelectric line at .04 sec past the J-point• Inverted T waves are always normal in aVR and may be normal in III and V1
    103. 103. Injury• Injured tissue does not depolarize completely and remains more positive than other tissue• ST segment is elevated more than 1mm above the baseline at 0.04 sec after the J-point in 2 or more related leads
    104. 104. Infarction• Q waves must be wider the 0.04 sec &/or greater than 25% of the height of the R wave• Q waves may be normal in III and aVR• Small Q waves in I, aVL, V5 and V6 are not infarction but are septal depolarization• Q waves in the V leads is also known as poor R wave progression
    105. 105. Reciprocal Changes• Mirror image that occurs when two electrodes view the AMI from opposite angles – Tall, upright T waves – ST seg depression – Taller R waves• May or may not be present and may indicate more severe damage
    106. 106. Evolution of MI
    107. 107. Reciprocal Leads and Their Corresponding Locations
    108. 108. Inferior Wall MI• May involve RV and/or LV• Usually RCA and sometimes LCx• Indicative changes: II, III, aVF• Reciprocal changes: I, aVL – Sometimes anterior precordial leads
    109. 109. Inferior Wall MI
    110. 110. Right Ventricular(inferior) Infarction
    111. 111. Inferior MI• Bradycardia• Atrial fib• AV Blocks: – 1st degree, 2nd degree type I, 3rd degree with junctional escape mechanism• Hypotension (treat with fluids)• Possible NTG, Morphine intolerance• Hiccoughs, Vomiting, JVD• Will Have clear lungs• Possible RV failure (RCA involved)
    112. 112. Anterior MI• Left ventricle• Involves the LAD• Indicative changes: V1-4
    113. 113. Anterior MI
    114. 114. Anterior MI• Sinus tachycardia• AV blocks – 2nd degree II, 3rd degree with ventricular escape mechanism• Bundle Branch Blocks – Beware if RBBB b/c septal arteries are high in LAD and a lot of muscle has probable been damaged• LV failure• Pulmonary edema• Hypotension is bad sign
    115. 115. Lateral Wall MI• Left Ventricle• Involves the LCx• Indicative changes: I, aVL, V5-6• Reciprocal changes: II, III, aVF
    116. 116. Lateral Wall
    117. 117. Lateral Wall• Bradycardia• Possible junctional rhythms• Possibly AV Blocks – 1st degree – 2nd degree, type I – 3rd degree, junctional escape mechanism
    118. 118. Posterior Wall• Back of LV• Generally involves the LCx but may be PDA coming off RCA• Indicative changes: V7-9 (if you do posterior leads)• Reciprocal changes: (look for these as your best clues) – Tall R waves in V1-2 – ST depression in V1-2• Frequently paired with inferior MI
    119. 119. Posterior MI
    120. 120. Non-Q wave MI• Subendocardial MI• 30% of all MI’s• Non-specific ST-T wave changes without Q wave formation• Usually hemodynamically stable• Risk of “extension” is significant
    121. 121. Serum Cardiac Markers• CK-MB subfomes for Dx within 6 hrs of MI onset• cTnI and cTnT efficient for late Dx of MI• CK-MB subform plus cardiac-specific Troponin best combination• Do not rely solely on Troponins because they remain elevated for 7-14 days and compromise ability to diagnose recurrent infarction
    122. 122. MI Management and Treatment• Nitrates to improve coronary blood flow; venous pooling reduces cardiac output, O2 use, and decreased preload.• Morphine vasodilates and decreases preload and afterload. Decreases sympathetic tone causing a decreased HR and O2 consumption.• Beta-blockers decrease HR and contractility and increase diastolic filling time.• Calcium Channel Blockers produce dilation of the coronary arteries and collateral vessels, decreasing contractility and conduction.
    123. 123. Clot Prevention and Destruction• ASA & G2B3A – Inhibit platelet aggregation – Integrilin, aggrastat, repro, plavix, ticlin• Heparin / LMWH – Deactivates thrombin and factors IX, X, XI, XII. – Lovenox• Fibrinolytics – Activate plasminogen to plasmin – TPA, Retavase
    124. 124. Thrombolytics• Indications – New onset ST segment elevation MI• Contraindications – Relative: HTN, recent trauma, pregnancy – Absolute: Active internal bleeding, suspected aortic dissection, intracranial neoplasm, prior hemorrhagic CVA or any CVA <1 yr old.
    125. 125. Angioplasty• Best outcome if <90 minutes from onset• Treat chest pain• Inhibit clotting• Watch for bleeding and reocclusion post procedure. – Leg kept straight – Head of bed < 30 degrees elevation
    126. 126. Other Emergencies
    127. 127. Pericarditis• Inflammation of the pericardium, the membrane that surrounds the heart – May cause ST-segment elevation and T-wave flattening or inversion – ST-segment and T-wave changes tend to be throughout all leads of the ECG. – The T wave usually does not invert until the ST segment has returned to baseline.
    128. 128. Pericarditis• Diagnostics – Help determine etiology of pericarditis – White blood cells • Elevated in infection – ESR • Elevated in infection – EKG • Diffuse ST segment changes • PR segment depression • Inverted T waves
    129. 129. Pericarditis• Management – NSAIDs – Antibiotic therapy
    130. 130. Pericardial Effusion• Pathophysiology – Abnormal buildup of fluid in the pericardial sac – Secondary to: • Pericarditis • Trauma – Places pressure on heart, decreases diastolic filling pressures
    131. 131. Cardiomyopathies• Cardiac disorders whose dominant feature is pathologic change to the myocardium• Include: – Primary cardiomyopathies • No underlying cause identified – Secondary cardiomyopathies • Have demonstrable underlying cause• Three major categories – Dilated cardiomyopathies – Hypertrophic cardiomyopathies – Restrictive cardiomyopathies
    132. 132. Dilated Cardiomyopathy• Pathophysiology – Myocardium enlarged, dilated – All four chambers can be involved – Often idiopathic – Toxic, metabolic, infectious factors may be involved – Decreased SV, EF = Increased end systolic volume – Increased end systolic volume = Increased end systolic pressure = Dilated chambers
    133. 133. Dilated Cardiomyopathy• Clinical manifestations – Fatigue, weakness – Progressive signs and symptoms of CHF – Right and left side – S3, S4 summation gallop – Mitral/tricuspid regurgitation murmurs
    134. 134. Dilated Cardiomyopathy• Diagnostics – Imaging studies • Radiograph – Cardiomegaly – Pulmonary edema – Pleural effusion • Echocardiogram – Dilated ventricle – EF <45 percent – ECG • Often nonspecific • BBB, intraventricular conduction delay
    135. 135. Dilated Cardiomyopathy• Management – Treat heart failure – Anticoagulants
    136. 136. Hypertrophic Cardiomyopathy (HCM)• Pathophysiology – Nondilated, hypertropic left ventricle – Unknown etiology – Thought to be genetic – Asymmetric thickening of septum, ventricular wall – Asymmetric tension on papillary muscles results in valvular regurgitation – Results in: • Decreased ventricular compliance • Decreased ventricular end diastolic volume • Increased pressure gradient
    137. 137. Hypertrophic Cardiomyopathy (HCM)• Clinical manifestations – Patients often asymptomatic – Systolic murmur – Dyspnea – Chest pain, angina, palpitations – Fatigue, weakness, vertigo, syncope
    138. 138. Hypertrophic Cardiomyopathy (HCM)• Diagnostics – Imaging • Radiograph • Left ventricular hypertrophy – ECG • Nonspecific intraventricular conduction • Bundle branch block – Echocardiogram • Decreased left ventricular ejection fraction
    139. 139. Hypertrophic Cardiomyopathy (HCM)• Management – Pharmacology – Beta-blockers – Calcium channel blockers
    140. 140. Restrictive Cardiomyopathy• Pathophysiology – Ventricular stiffness leads to diastolic dysfunction – Resembles constrictive pericarditis – Progressive limitation of ventricular filling secondary to endocardial and myocardial lesions • Scarring – Reduced cardiac output
    141. 141. Restrictive Cardiomyopathy• Clinical manifestations – Chest pain – Dyspnea with exertion – Exercise intolerance – Evidence of right ventricular failure – JVD – Hepatomegaly – Ascities – Anasarca – Mitral/tricuspid murmurs, S3 and S4 sounds
    142. 142. Restrictive Cardiomyopathy• Diagnostics – Radiograph • Pulmonary congestion – ECG • Sinus tachycardia • Atrial fibrillation • Biventricular hypertrophy
    143. 143. Restrictive Cardiomyopathy• Management – Fluid restriction – Diuretic therapy – Antidysrhythmic therapy
    144. 144. Aortic Stenosis• Pathophysiology – Opening of aortic valve is narrowed and obstructs forward blood flow into aorta – Left ventricle attempts to increase SV and CO – Results in left ventricular hypertrophy• Clinical manifestations – Typically presents with triad of: • Angina, Exertional syncope, Dyspnea on exertion – Left Axis Deviation, Left Hypertrophy• Treatment includes nitrates, diuretics, digitalis, IABP as bridge to surgery
    145. 145. Aortic Regurgitation / Insufficiency• Pathophysiology – Leaking aortic valve – Rising left ventricular pressures result in: • Left ventricular dilation, Left ventricular hypertrophy, Left heart failure• Presentation – CHF, Hypotension, Angina, Wide Pulse Pressure, Corrigan’s Pulse• Treatment – surgical repair
    146. 146. Mitral Stenosis• Stenotic valve obstructs forward blood flow from the left atrium into the left ventricle• Results in elevated left atrial pressure• Pulmonary hypertension – Right ventricle can fail• Rheumatic fever most common cause• Clinical presentation – Exertional dyspnea, orthopnea, fatigue, malaise, palpable diastolic thrill
    147. 147. Mitral Stenosis• Management – Treat symptoms of congestive heart failure – Use diuretics – Give nitrates – Treat atrial fibrillation – Conduct digitalis – Complete anticoagulation for new-onset atrial fibrillation – Intervene surgically
    148. 148. Hyperkalemia• Elevated potassium level (normal 3.5 – 5 mEq/L)• Diagnostic criteria – T-wave abnormalities (tall and peaked) – Intraventricular conduction delays – P-wave abnormalities (missing or decreased amplitude) – ST-segment changes simulating an injury pattern – Cardiac arrhythmias (predominantly bradycardias) – Sinusoidal ECG pattern
    149. 149. Hypokalemia• Decreased level of potassium• Diagnostic criteria – ST-segment depression – Slightly decreased amplitude of the T waves – Minimal prolongation of the QRS interval – U wave is usually small and follows the T wave.
    150. 150. Hypercalcemia• Elevated levels of calcium (normal 8.5 – 10.5 mg/dl)• Diagnostic criteria – Shortening of the ST-segment, which, in turn, shortens the QT interval – PR interval may be prolonged – QRS may lengthen – T waves may become flat or invert
    151. 151. Hypocalcemia• Reduced levels of calcium• Diagnostic criteria – A prolongation of the ST segment that produces a lengthening of the QT interval
    152. 152. Coronary Artery Spasm• Variant or Prinzmetal’s angina• May occur spontaneously or: – Exposure to cold – Emotional stress – Vasoconstricting meds – Cocaine – Smoking• Mimics MI
    153. 153. QUESTIONS?