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Cardiology part 1
Cardiology part 1
Cardiology part 1
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Cardiology part 1

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  • In order to survive a heart attack, a victim must recognize the symptoms quickly and medical care must be started within an hour of onset of symptoms. What are some risk factors of heart disease? Smoking Older age Family history Htn High cholesterol Diabetes Cocaine use Male Diet Obesity Oral contraceptives Sedentary life style Type a personality Stress
  • Test Question: What are the three layers of the heart The myocardium has a unique ability to cnduct electrical impulses, causing the heart to contract.
  • Test Question : Oxygenated blood returns to the heart through ? Test Question: Left side of heart does more work therefore thicker walls.
  • Test Question: Heart receives its nutrients from coronary arteries
  • Poiseuille’s law states that flow through vessel is directly proportional to the radius of the vessel to the fourth power
  • Test Question: The period of time from one cardian contraction to the next is called? Test Question: Pressure in the filled ventricle at the end of diastole is called Preload. Remember starling’s law Test Question: Equation to determine cardiac output is stroke volume x heart rate (sv=70ml) co = 5 L/m Ejection fraction – ventricle ejects 2/3 volume of blood it contains, this is known as stroke volume Afterload is the peripheral resistance that the heart must pump against. Higher pressure results in lower stroke volume
  • Sympathetic and parasympathetic system work in opposition to maintain balance Dromotropy refers to the rate of nervous impulses to the heart. Electrolytes Na+ Ca++ K+ Cl- Mg+
  • Intercalated disks are fibers inside the cell that conduct electrical impulses to the next cell. A group of these is called synctium. There are 2 synctium atrial and ventricular. Atria depolarize from superior to infefrior to push blood into ventricles. Ventricles depolarize opposite. Conduction between atria and ventricles must pass through AV bindle
  • Test Question: Depolorization is the opposite of the cell’s resting state. The opposite is repolarization Normally while resting, the cell pumps Na+ outside the cell leaving the inside of the cell more negatively charged This is called resting potential When stimulated, the membrance changes allowing Na+ to rush into the cell causing the cell to become more + charged. This is called depolarization and results in an action potential Potassium K+ escapes from the cell causing the cell to return to resting potential and is called repolarization.
  • Test Question: SA node’s intrinsic rate of self exitation AV junction slows conduction allows ventricles time to fill. Purkinge 15 -40 bpm.
  • Absence of electrical impulse is an isoelectric line
  • Test Question: Bipolar Limb leads and what is Einthoven’s triangle Any electrical impulse moving toward the positive lead will result in an upward deflection on the ecg. No deflection may mean that current is flowing perpendicular to lead. That’s why we use 12 leads.
  • Speed 25 mm/sec Light lines 1 mm apart, heavy lines are 5 mm apart. etc
  • Test Question: The interval of time in the cardiac cycle when a sufficiently strong stimulus may produce depolarization is called the relative refractory period.
  • Transcript

    • 1. Cardiology
    • 2. Part 1: CardiovascularAnatomy & Physiology, ECG Monitoring, and Dysrhythmia Analysis
    • 3. Sections Cardiovascular Anatomy Cardiac Physiology Electrocardiographic Monitoring Dysrhythmias
    • 4. Cardiovascular Anatomy Anatomy of the Heart  Location and Size of the Heart
    • 5. Cardiovascular Anatomy Tissue Layers  Endocardium  Myocardium  Pericardium • Visceral Pericardium • Parietal Pericardium • Pericardial Fluid
    • 6. Cardiovascular Anatomy Valves  Atrioventricular Valves • Tricuspid Valve • Mitral Valve  Semilunar Valves • Aortic Valve • Pulmonic Valve  Chordae Tendonae
    • 7. Cardiovascular Anatomy Blood Flow  From the Body • Right Atrium  To the Lungs • Right Ventricle  From the Lungs • Left Atrium  To the Body • Left Ventricle
    • 8. Cardiovascular Anatomy  Coronary Circulation  Collateral Circulation
    • 9. Cardiovascular Anatomy Anatomy of the Peripheral Circulation  General Structure  Poiseuille’s Law  Arterial System  Arteries, arterioles, and capillaries  Venous System  Capillaries, venules, and veins
    • 10. Cardiac Physiology The Cardiac Cycle  Diastole  Systole  Ejection Fraction  Stroke Volume • Preload • Cardiac Contractility • Afterload  Cardiac Output
    • 11. Cardiac Physiology Nervous Control of the Heart  Sympathetic  Parasympathetic  Autonomic Control of the Heart  Chronotropy  Inotropy  Dromotropy  Role of Electrolytes
    • 12. Cardiac Physiology Electrophysiology  Cardiac Muscle  Atrial  Ventricular  Excitatory and Conductive Fibers • Intercalated discs • Syncytium  Atrioventricular Bundle  Depolarization
    • 13. Cardiac Physiology Cardiac Depolarization  Resting Potential  Action Potential  Repolarization
    • 14. Cardiac Physiology Cardiac Conductive System  Properties • Excitability • Conductivity • Automaticity • Contractility
    • 15. Cardiac Physiology Cardiac Conductive System  Components • Sinoatrial Node • Internodal Atrial Pathways • Atrioventricular Node • Atrioventricular Junction • Bundle of His • Left and Right Bundle Branches • Purkinje Fibers
    • 16. Electrocardiographic Monitoring The Electrocardiogram  Positive and Negative Impulses  The Isoelectric Line  Artifact  Muscle tremors  Shivering  Patient movement  Loose electrodes  60 Hertz interference  Machine malfunction
    • 17. The Electrocardiogram ECG Leads  Bipolar (Limb)  Einthoven’s Triangle  Leads I, II, III  Augmented (Unipolar)  aVR, aVL, aVF  Precordial  V1 – V6
    • 18. The Electrocardiogram Routine Monitoring  Information from a single lead shows:  Rate & regularity.  Time to conduct an impulse.  A single lead cannot:  Identify/locate an infarct.  Identify axis deviation or chamber enlargement.  Identify right-to-left differences in conduction.  The quality or presence of pumping action.
    • 19. The Electrocardiogram ECG Paper  Speed  Amplitude and Deflection  Calibration
    • 20. The Electrocardiogram Relationship of the ECG to Electrical Events in the Heart  ECG Components  P Wave  QRS Complex  T Wave  U Wave
    • 21. The Electrocardiogram
    • 22. The Electrocardiogram
    • 23. The Electrocardiogram
    • 24. The Electrocardiogram
    • 25. The Electrocardiogram
    • 26. The Electrocardiogram
    • 27. The Electrocardiogram
    • 28. The Electrocardiogram Time Intervals  P–R Interval (PRI) or P–Q Interval (PQI) • 0.12–0.20 Seconds  QRS Interval • 0.08–0.12 Seconds  S–T Segment  Q–T Interval • 0.33–0.42 Seconds
    • 29. The Electrocardiogram Refractory Periods  Absolute  Relative
    • 30. The Electrocardiogram S–T Segment Changes  Associated with Myocardial Infarctions  Ischemia  Injury  Necrosis
    • 31. The Electrocardiogram Lead Systems and Heart Surfaces
    • 32. The Electrocardiogram Interpretation of Rhythm Strips  Basic Criteria  Always be consistent and analytical.  Memorize the rules for each dysrhythmia.  Analyze a given rhythm strip according to a specific format.  Compare your analysis to the rules for each dysrhythmia.  Identify the dysrhythmia by its similarity to established rules.
    • 33. The Electrocardiogram Five-Step Procedure  Analyze the rate.  Analyze the rhythm.  Analyze the P-waves.  Analyze the P–R interval.  Analyze the QRS complex.
    • 34. The Electrocardiogram Analyzing Rate  Six-Second Method  Heart Rate Calculator Rulers  R–R Interval  Triplicate Method Analyzing Rhythm  Regular  Occasionally Irregular  Regularly Irregular  Irregularly Irregular
    • 35. The Electrocardiogram Analyzing P Waves  Are P waves present?  Are the P waves regular?  Is there one P wave for each QRS complex?  Are the P waves upright or inverted?  Do all the P waves look alike? Analyzing the P–R Interval Analyzing the QRS Complex  Do all the QRS complexes look alike?  What is the QRS duration?
    • 36. Dysrhythmias Normal Sinus Rhythm  Rate  60–100  Rhythm  Regular  P waves  Normal, upright, only before each QRS complex  PR Interval  0.12–0.20 seconds  QRS Complex  Normal, duration of <0.12 seconds
    • 37. Causes of Dysrhythmias Myocardial  Trauma to the Ischemia, Necrosis, Myocardium or Infarction  Drug Effects and Autonomic Nervous Drug Toxicity System Imbalance  Electrocution Distention of the  Hypothermia Chambers of the  CNS Damage Heart  Idiopathic Blood Gas Events Abnormalities  Normal Electrolyte Occurrences Imbalances
    • 38. Dysrhythmias Dysrhythmia Arrhythmia Mechanism of Impulse Formation  Ectopic Foci  Ectopic Beats  Reentry
    • 39. Dysrhythmias Classification of Dysrhythmias  Nature of Origin  Magnitude  Severity  Site of Origin
    • 40. Dysrhythmias Classification by Site of Origin  Dysrhythmias Originating in the SA Node  Dysrhythmias Originating in the Atria  Dysrhythmias Originating Within the AV Junction (AV Blocks)  Dysrhythmias Sustained in or Originating in the AV Junction  Dysrhythmias Originating in the Ventricles  Dysrhythmias Resulting from Disorders of Conduction
    • 41. Dysrhythmias Originating in the SA Node Sinus Bradycardia Sinus Tachycardia Sinus Dysrhythmia Sinus Arrest
    • 42. Dysrhythmias Originating in the SA Node Rules of Interpretation Sinus BradycardiaRate Less than 60Rhythm RegularPacemaker Site SA nodeP Waves Upright & normalPRI NormalQRS Normal
    • 43. Dysrhythmias Originating in the SA Node Sinus Bradycardia  Etiology  Increased parasympathetic (vagal) tone, intrinsic disease of the SA node, drug effects.  May be a normal finding in healthy, well-conditioned persons.  Clinical Significance  May result in decreased cardiac output, hypotension, angina, or CNS symptoms.  In healthy, well-conditioned person, may have no significance.  Treatment  Generally unnecessary unless hypotension or ventricular irritability is present.
    • 44. Dysrhythmias Originating in the SA Node Sinus Bradycardia  Treatment
    • 45. Dysrhythmias Originating in the SA Node Rules of Interpretation Sinus TachycardiaRate Greater than 100Rhythm RegularPacemaker Site SA nodeP Waves Upright & normalPRI NormalQRS Normal
    • 46. Dysrhythmias Originating in the SA Node Sinus Tachycardia  Etiology  Results from an increased rate of SA node discharge.  Potential causes include exercise, fever, anxiety, hypovolemia, anemia, pump failure, increased sympathetic tone, hypoxia, or hypothyroidism.  Clinical Significance  Decreased cardiac output for rates >140.  Very rapid rates can precipitate ischemia or infarct.  Treatment  Treatment is directed at the underlying cause.
    • 47. Dysrhythmias Originating in the SA Node Rules of Interpretation Sinus DysrhythmiaRate 60–100Rhythm IrregularPacemaker Site SA nodeP Waves Upright & normalPRI NormalQRS Normal
    • 48. Dysrhythmias Originating in the SA Node Sinus Dysrhythmia  Etiology  Often a normal finding, sometimes related to the respiratory cycle.  May be caused by enhanced vagal tone.  Clinical Significance  Normal variant.  Treatment  Typically, none required.
    • 49. Dysrhythmias Originating in the SA Node Rules of Interpretation Sinus ArrestRate Normal to slowRhythm IrregularPacemaker Site SA nodeP Waves Upright & normalPRI NormalQRS Normal
    • 50. Dysrhythmias Originating in the SA Node Sinus Arrest  Etiology  Occurs when the sinus node fails to discharge.  May result from ischemia of the SA node, digitalis toxicity, excessive vagal tone, or degenerative fibrotic disease.  Clinical Significance  Frequent or prolonged episodes may decrease cardiac output and cause syncope.  Prolonged episodes may result in escape rhythms.  Treatment  None if patient is asymptomatic.  Treat symptomatic bradycardia.
    • 51. Dysrhythmias Originating in the Atria Atrial Tachycardia Multifocal Atrial Tachycardia Premature Atrial Contractions Paroxysmal Supraventricular Tachycardia Atrial Flutter Atrial Fibrillation
    • 52. Dysrhythmias Originating in the Atria Rules of Interpretation Atrial TachycardiaRate Usually normalRhythm Slightly irregular Varies among the SAPacemaker node, atrial tissue,Site and AV JunctionP Waves Variable or absent Varies depending onPRI source of impulseQRS Normal
    • 53. Dysrhythmias Originating in the Atria Atrial Tachycardia  Etiology  Variant of sinus dysrhythmia, which is a natural phenomenon in the very young or old.  May also be caused by ischemic heart disease or atrial dilation.  Clinical Significance  None, but may be precursor to other atrial dysrhythmias.  Treatment  Typically, none required.
    • 54. Dysrhythmias Originating in the Atria Rules of Interpretation Multifocal Atrial TachycardiaRate More than 100Rhythm IrregularPacemaker Site Ectopic sites in atria Organized, nonsinus PP Waves waves; at least 3 forms Varies depending onPRI source of impulseQRS Variable
    • 55. Dysrhythmias Originating in the Atria Multifocal Atrial Tachycardia  Etiology  Often seen in acutely ill patients.  May result from pulmonary disease, metabolic disorders, ischemic heart disease, or recent surgery.  Clinical Significance  Presence of multifocal atrial tachycardia often indicates a serious underlying illness.  Treatment  Treat the underlying illness.
    • 56. Dysrhythmias Originating in the Atria Rules of InterpretationPremature Atrial Contractions Depends onRate underlying rhythm Usually regularRhythm except for the PACPacemaker Site Ectopic sites in atria Occurs earlier thanP Waves expected Varies dependent onPRI foci of impulseQRS Usually normal
    • 57. Dysrhythmias Originating in the Atria Premature Atrial Contractions  Etiology  Single electrical impulse originating outside the SA node.  May result from use of caffeine, tobacco, or alcohol, sympathomimetic drugs, ischemic heart disease, hypoxia, or digitalis toxicity, or may be idiopathic.  Clinical Significance  None. Presence of PACs may be a precursor to other atrial dysrhythmias.  Treatment  None if asymptomatic. Treat symptomatic patients by administering high-flow oxygen and establishing IV access.
    • 58. Dysrhythmias Originating in the Atria Rules of Interpretation Paroxysmal Supraventricular TachycardiaRate 150–250Rhythm RegularPacemaker Atrial (outside SA Node)Site Often buried inP Waves preceding T wavePRI Usually normalQRS Usually normal
    • 59. Dysrhythmias Originating in the Atria Paroxysmal Supraventricular Tachycardia  Etiology  Rapid atrial depolarization overrides the SA node.  May be precipitated by stress, overexertion, smoking, caffeine.  Clinical Significance  May be tolerated well by healthy patients for short periods.  Marked reduction in cardiac output can precipitate angina, hypotension, or congestive heart failure.
    • 60. Dysrhythmias Originating in the Atria Paroxysmal Supraventricular Tachycardia  Treatment  Vagal Maneuvers  Pharmacological Therapy • Adenosine • Verapamil  Electrical Therapy • Consider if patient symptomatic with HR > 150. • Synchronized cardioversion starting at 100J.
    • 61. Tachycardia Algorithm
    • 62. Dysrhythmias Originating in the Atria Rules of Interpretation Atrial Flutter Atrial rate 250–350Rate Ventricular rate variesRhythm Usually regularPacemaker Site Atrial (outside SA node)P Waves F waves are presentPRI Usually normalQRS Usually normal
    • 63. Dysrhythmias Originating in the Atria Atrial Flutter  Etiology  Results when the AV node cannot conduct all the impulses.  Impulses may be conducted in fixed or variable ratios.  Usually associated with organic disease such as congestive heart failure (rarely seen with MI).  Clinical Significance  Generally well tolerated.  Rapid ventricular rates may compromise cardiac output and result in symptoms.  May occur in conjunction with atrial fibrillation.
    • 64. Dysrhythmias Originating in the Atria Atrial Flutter  Treatment  Electrical Therapy • Consider if ventricular rate > 150 and symptomatic. • Synchronized cardioversion starting at 100J.  Pharmacological Therapy • Diltiazem. • Verapamil, digoxin, beta-blockers, procainamide, and quinidine.
    • 65. Dysrhythmias Originating in the Atria Rules of Interpretation Atrial Fibrillation Atrial rate 350–50Rate Ventricular rate variesRhythm Irregularly irregularPacemaker Site Atrial (outside SA Node)P Waves None discerniblePRI NoneQRS Normal
    • 66. Dysrhythmias Originating in the Atria Atrial Fibrillation  Etiology  Results from multiple ectopic foci; AV conduction is random and highly variable.  Often associated with underlying heart disease.  Clinical Significance  Atria fail to contract effectively, reducing cardiac output.  Well tolerated with normal ventricular rates.  High or low ventricular rates can result in cardiac compromise.
    • 67. Dysrhythmias Originating in the Atria Atrial Flutter  Treatment  Electrical Therapy • Consider if ventricular rate > 150 and symptomatic. • Synchronized cardioversion starting at 100J.  Pharmacological Therapy • Diltiazem. • Verapamil, digoxin, beta blockers, procainamide, and quinidine. • Anticoagulant (heparin or warfarin).
    • 68. Dysrhythmias Originating Within the AV Junction (AV Blocks) AV Blocks  Locations  At the AV Node  At the Bundle of His  Below the Bundle of His  Classifications  First-Degree AV Block  Type I Second-Degree AV Block  Type II Second-Degree AV Block  Third-Degree AV Block
    • 69. Dysrhythmias Originating Within the AV Junction (AV Blocks) Rules of Interpretation First-Degree AV Block Depends onRate underlying rhythmRhythm Usually regularPacemaker Site SA node or atrialP Waves NormalPRI > 0.20 Seconds Usually < 0.12QRS seconds
    • 70. Dysrhythmias Originating Within the AV Junction (AV Blocks) First-Degree AV Block  Etiology  Delay in the conjunction of an impulse through the AV node.  May occur in healthy hearts, but often indicative of ischemia at the AV junction.  Clinical Significance  Usually not significant, but new onset may precede a more advanced block.  Treatment  Generally, none required other than observation.  Avoid drugs that may further slow AV conduction.
    • 71. Dysrhythmias Originating Within the AV Junction (AV Blocks) Rules of Interpretation Type I Second-Degree AV Block Atrial, normal;Rate ventricular, normal to slow Atrial, regular;Rhythm ventricular, irregularPacemaker Site SA node or arial Normal, some P wavesP Waves not followed by QRS Increases until QRS isPRI dropped, then repeatsQRS Usually < 0.12 seconds
    • 72. Dysrhythmias Originating Within the AV Junction (AV Blocks) Type I Second-Degree AV Block  Etiology  Also called Mobitz I, or Wenckebach.  Delay increases until an impulse is blocked.  Indicative of ischemia at the AV junction.  Clinical Significance  Frequently dropped beats can result in cardiac compromise.  Treatment  Generally, none required other than observation.  Avoid drugs that may further slow AV conduction.  Treat symptomatic bradycardia.
    • 73. Dysrhythmias Originating Within the AV Junction (AV Blocks) Rules of Interpretation Type II Second-Degree AV Block Atrial, normal;Rate ventricular, slow May be regular orRhythm irregularPacemaker Site SA node or atrial Normal, some P wavesP Waves not followed by QRS Constant for conducted beats, mayPRI be > 0.21 secondsQRS Normal or > 0.12 seconds
    • 74. Dysrhythmias Originating Within the AV Junction (AV Blocks) Type II Second-Degree AV Block  Etiology  Also called Mobitz II or infranodal.  Intermittent block of impulses.  Usually associated with MI or septal necrosis.  Clinical Significance  May compromise cardiac output and is indicative of MI.  Often develops into full AV blocks.  Treatment  Avoid drugs that may further slow AV conduction.  Treat symptomatic bradycardia.  Consider transcutaneous pacing.
    • 75. Dysrhythmias Originating Within the AV Junction (AV Blocks) Rules of Interpretation Third-Degree AV Block Atrial, normal;Rate ventricular, 40–60 Both atrial andRhythm ventricular are regular SA node and AVPacemaker Site junction or ventricle Normal,with noP Waves correlation to QRSPRI No relationship to QRSQRS 0.12 seconds or greater
    • 76. Dysrhythmias Originating Within the AV Junction (AV Blocks) Third-Degree AV Block  Etiology  Absence of conduction between the atria and the ventricles.  Results from AMI, digitalis toxicity, or degeneration of the conductive system.  Clinical Significance  Severely compromised cardiac output.  Treatment  Transcutaneous pacing for acutely symptomatic patients.  Treat symptomatic bradycardia.  Avoid drugs that may further slow AV conduction.
    • 77. Dysrhythmias Sustained or Originating in the AV Junction Dysrhythmias  Premature Junctional Contractions  Junctional Escape Complexes and Rhythm  Accelerated Junctional Rhythm  Paroxysmal Junctional Tachycardia Characterisitics  Inverted P Waves in Lead II  PRI of < 0.12 Seconds  Normal QRS Complex Duration
    • 78. Dysrhythmias Sustained or Originating in the AV Junction Rules of Interpretation Premature Junctional Contractions Depends on underlyingRate rhythm Depends on underlyingRhythm rhythm Ectopic focus in the AVPacemaker Site junction Inverted, may occur afterP Waves QRS Normal if P occursPRI before QRSQRS Usually normal
    • 79. Dysrhythmias Sustained or Originating in the AV Junction Premature Junctional Contractions  Etiology  Single electrical impulse originating in the AV node.  May occur with use of caffeine, tobacco, alcohol, sympathomimetic drugs, ischemic heart disease, hypoxia, or digitalis toxicity, or may be idiopathic.  Clinical Significance  Limited, frequent PJCs may precursor other junctional dysrhythmias.  Treatment  None usually required.
    • 80. Dysrhythmias Sustained or Originating in the AV Junction Rules of Interpretation Junctional Escape Complexes and RhythmsRate 40–60 Irregular in singleRhythm occurrence, regular in escape rhythmPacemaker Site AV junction Inverted, may occur afterP Waves QRS Normal if P occursPRI before QRSQRS Usually normal
    • 81. Dysrhythmias Sustained or Originating in the AV Junction Junctional Escape Complexes and Rhythms  Etiology  Results when the AV node becomes the pacemaker.  Results from increased vagal tone, pathologically slow SA discharges, or heart block.  Clinical Significance  Slow rate may decrease cardiac output, precipitating angina and other problems.  Treatment  None if the patient remains asymptomatic.  Treat symptomatic episodes with atropine or pacing as indicated.
    • 82. Dysrhythmias Sustained or Originating in the AV Junction Rules of InterpretationAccelerated Junctional RhythmRate 60–100Rhythm RegularPacemaker Site AV junction Inverted, may occurP Waves after QRS Normal if P occursPRI before QRSQRS Normal
    • 83. Dysrhythmias Sustained or Originating in the AV Junction Accelerated Junctional Rhythm  Etiology  Results from increased automaticity in the AV junction.  Often occurs due to ischemia of the AV junction.  Clinical Significance  Usually well tolerated, but monitor for other dysrhythmias.  Treatment  None generally required in the prehospital setting.
    • 84. Dysrhythmias Sustained or Originating in the AV Junction Rules of Interpretation Paroxysmal Junctional TachycardiaRate 100–180Rhythm RegularPacemaker Site AV junction Inverted, may occurP Waves after QRS Normal if P occursPRI before QRSQRS Normal
    • 85. Dysrhythmias Sustained or Originating in the AV Junction Paroxysmal Junctional Tachycardia  Etiology  Rapid AV junction depolarization overrides the SA node.  Occurs with or without heart disease.  May be precipitated by stress, overexertion, smoking, or caffeine ingestion.  Clinical Significance  May be well tolerated for brief periods.  Decreased cardiac output will result from prolonged episodes, which may precipitate angina, hypotension, or congestive heart failure.
    • 86. Dysrhythmias Sustained or Originating in the AV Junction Paroxysmal Junctional Tachycardia  Treatment  Vagal Maneuvers  Pharmacological Therapy • Adenosine • Verapamil  Electrical Therapy • Use if rate is > 150 and patient is hemodynamically unstable. • Synchronized cardioversion starting at 100J.
    • 87. Dysrhythmias Originating in the Ventricles Dysrhythmias  Ventricular Escape Complexes and Rhythms  Accelerated Idioventricular Rhythm  Premature Ventricular Contractions  Ventricular Tachycardia  Related Dysrhythmia  Ventricular Fibrillation  Asystole  Artificial Pacemaker Rhythm
    • 88. Dysrhythmias Originating in the Ventricles Rules of Interpretation Ventricular Escape Complexes and RhythmsRate 15–40 Escape complex, irregular;Rhythm escape rhythm, RegularPacemaker Site VentricleP Waves NonePRI NoneQRS >0.12 seconds, bizarre
    • 89. Dysrhythmias Originating in the Ventricles Ventricular Escape Complexes and Rhythms  Etiology  Safety mechanism to prevent cardiac standstill.  Results from failure of other foci or high-degree AV block.  Clinical Significance  Decreased cardiac output, possibly to life-threatening levels.  Treatment  For perfusing rhythms, administer atropine and/or TCP.  For nonperfusing rhythms, follow pulseless electrical activity (PEA) protocols.
    • 90. Dysrhythmias Originating in the Ventricles Accelerated Idioventricular Rhythm  Etiology  A subtype of ventricular escape rhythm that frequently occurs with MI.  Ventricular escape rhythm with a rate of 60–110.  Clinical Significance  May cause decreased cardiac output if the rate slows.  Treatment  Does not usually require treatment unless the patient becomes hemodynamically unstable.  Primary goal is to treat the underlying MI.
    • 91. Dysrhythmias Originating in the Ventricles Rules of Interpretation Premature Ventricular ContractionsRate Underlying rhythm Interrupts regularRhythm underlying rhythmPacemaker Site VentricleP Waves NonePRI NoneQRS >0.12 seconds, bizarre
    • 92. Dysrhythmias Originating in the Ventricles Premature Ventricular Contractions  Etiology  Single ectopic impulse resulting from an irritable focus in either ventricle.  Causes may include myocardial ischemia, increased sympathetic tone, hypoxia, idiopathic causes, acid–base disturbances, electrolyte imbalances, or as a normal variation of the ECG.  May occur in patterns • Bigeminy, trigeminy, or quadrigeminy. • Couplets and triplets.
    • 93. Dysrhythmias Originating in the Ventricles Premature Ventricular Contractions  Clinical Significance  Malignant PVCs • More than 6/minute, R on T phenomenon, couplets or runs of ventricular tachycardia, multifocal PVCs, or PVCs associated with chest pain.  Ventricles do not adequately fill, causing decreased cardiac output.
    • 94. Dysrhythmias Originating in the Ventricles Premature Ventricular Contractions  Treatment  Non-malignant PVCs do not usually require treatment in patients without a cardiac history.  Cardiac patient with nonmalignant PVCs . • Administer oxygen and establish IV access  Malignant PVCs: • Lidocaine 1.0 –1.5 mg/kg IV bolus. • If PVCs are not suppressed, repeat doses of 0.5-0.75 mg/kg to max dose of 3.0 mg/kg. • If PVCs are suppressed, administer lidocaine drip 2–4 mg/min. • Reduce the dose in patients with decreased output or decreased hepatic function and patients > 70 years old.
    • 95. Dysrhythmias Originating in the Ventricles Rules of Interpretation Ventricular TachycardiaRate 100–250Rhythm Usually regularPacemaker Site Ventricle If present, notP Waves associated with QRSPRI NoneQRS >0.12 seconds, bizarre
    • 96. Dysrhythmias Originating in the Ventricles Ventricular Tachycardia  Etiology  3 or more ventricular complexes in succession at a rate of >100.  Causes include myocardial ischemia, increased sympathetic tone, hypoxia, idiopathic causes, acid–base disturbances, or electrolyte imbalances.  VT may appear monomorphic or polymorphic  Clinical Significance  Decreased cardiac output, possibly to life-threatening levels.  May deteriorate into ventricular fibrillation.
    • 97. Dysrhythmias Originating in the Ventricles Ventricular Tachycardia  Treatment  Perfusing patient • Administer oxygen and establish IV access. • Consider immediate synchronized cardioversion starting at 100J for hemodynamically unstable patients. • Initially administer lidocaine 1.0–1.5 mg/kg IV. • Administer repeat doses of lidocaine 0.5–0.75 mg/kg to the max dose of 3.0 mg/kg, or until VT is suppressed. • Amiodarone 150–300 mg IV.  Nonperfusing patient • Follow ventricular fibrillation protocol.
    • 98. Dysrhythmias Originating in the Ventricles Torsade de Pointes  Polymorphic VT.  Caused by the use of certain antidysrhythmic drugs.  Exacerbated by coadministration of antihistamines, azole antifungal agents and macrolide antibiotics, erythromycin, azithromycin, and clarithramycin.
    • 99. Dysrhythmias Originating in the Ventricles Torsade de Pointes  Typically occurs in nonsustained bursts.  Prolonged Q–T interval during “breaks.”  QRS rates from 166–300.  RR interval highly variable.  Treatment  Do not treat as standard VT.  Administer magnesium sulfate 1–2 g diluted in 100 ml D5W over 1–2 minutes.  Amiodarone 150–300 mg is also effective.
    • 100. Dysrhythmias Originating in the Ventricles Rules of Interpretation Ventricular FibrillationRate No organized rhythmRhythm No organized rhythm NumerousPacemaker Site ventricular fociP Waves Usually absentPRI NoneQRS None
    • 101. Dysrhythmias Originating in the Ventricles Ventricular Fibrillation  Etiology  Wide variety of causes, often resulting from advanced coronary artery disease.  Clinical Significance  Lethal dysrhythmia with no cardiac output and no organized electrical pattern.
    • 102. Dysrhythmias Originating in the Ventricles Ventricular Fibrillation  Treatment  Initiate CPR.  Defibrillate with 200J, repeated with 200–300J and 360J if the rhythm does not convert.  Control the airway and establish IV access.  Administer epinephrine 1:10,000 every 3–5 minutes.  Consider second-line drugs such as lidocaine, bretylium, amiodarone, procainamide, or magnesium sulfate.  Consider 40 IU Vasopressin IV (one time only).
    • 103. Dysrhythmias Originating in the Ventricles Rules of Interpretation AsystoleRate No Electrical ActivityRhythm No Electrical ActivityPacemaker Site No Electrical ActivityP Waves AbsentPRI AbsentQRS Absent
    • 104. Dysrhythmias Originating in the Ventricles Asystole  Etiology  Primary event in cardiac arrest, resulting from massive myocardial infarction, ischemia, and necrosis.  Final outcome of ventricular fibrillation.  Clinical Significance  Asystole results in cardiac arrest.  Poor prognosis for resuscitation.
    • 105. Dysrhythmias Originating in the Ventricles Asystole  Treatment  Administer CPR and manage the airway.  Treat for ventricular fibrillation if there is any doubt about the underlying rhythm.  Administer medications • Epinephrine, atropine, and possibly sodium bicarbonate.
    • 106. Dysrhythmias Originating in the Ventricles
    • 107. Dysrhythmias Originating in the Ventricles Rules of InterpretationArtificial Pacemaker Rhythm Varies withRate pacemaker May be regular orRhythm irregularPacemaker Depends uponSite electrode placement None produced byP Waves ventricular pacemakers; pacemaker spikePRI If present, variesQRS >0.12 seconds, bizarre
    • 108. Dysrhythmias Originating in the Ventricles Artificial Pacemaker Rhythm  Etiology  Single vs. dual chamber pacemakers.  Fixed-rate vs. demand pacemakers.  Clinical Significance  Used in patients with a chronic high-–grade heart block, sick sinus syndrome, or severe symptomatic bradycardia.
    • 109. Dysrhythmias Originating in the Ventricles Artificial Pacemaker Rhythm  Problems with Pacemakers  Battery failure  “Runaway” pacers  Displaced leads  Management Considerations  Identify patients with pacemakers.  Treat the patient.  Use of a Magnet
    • 110. Pulseless Electrical Activity Characteristics  Electrical impulses are present, but with no accompanying mechanical contractions of the heart.  Treat the patient, not the monitor. Causes  Hypovolemia, cardiac tamponade, tension pneumothorax, hypoxemia, acidosis, massive pulmonary embolism, ventricular wall rupture.
    • 111. Pulseless Electrical Treatment Activity  Prompt recognition and early treatment.  Epinephrine 1 mg every 3–5 minutes.  Treat underlying cause of PEA.
    • 112. PulselessElectricalActivity
    • 113. Dysrhythmias Resulting from Disorders of Conduction Categories of Conductive Disorders  Atrioventricular Blocks  Disturbances of Ventricular Conduction  Preexcitation Syndromes
    • 114. Dysrhythmias Resulting from Disorders of Conduction Disturbances of Ventricular Conduction  Aberrant Conduction  Bundle Branch Block  Causes  Ischemia or necrosis of a bundle branch  PAC or PJC that reaches one of the bundle branches in a refractory period  Differentiation of SVT and Wide-Complex Tachycardias
    • 115. Dysrhythmias Resulting from Disorders of Conduction Pre-excitation Syndromes  Excitation by an impulse that bypasses the AV node  Wolff-Parkinson- White Syndrome (WPW) • Short PRI and long QRS duration • Delta waves  Treat underlying rhythm.
    • 116. ECG Changes Due to ElectrolyteAbnormalities and Hypothermia Hyperkalemia  Tall Ts  Suspect in patients with a history of renal failure. Hypokalemia  Prominent U waves Hypothermia  Osborn wave (“J” wave)  T wave inversion, sinus bradycardia, atrial fibrillation or flutter, AV blocks, PVCs, VF, asystole
    • 117. Cardiology Cardiovascular Anatomy Cardiac Physiology Electrocardiographic Monitoring Dysrhythmias

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