A Review of Cardiac Pathophysiology and EKG. Jamie Dyson PT, DPT Kathy Swanick PT, DPT, OCS

Transcription

1 A Review of Cardiac Pathophysiology and EKG Jamie Dyson PT, DPT Kathy Swanick PT, DPT, OCS

2 Cardiac Pathophysiology Coronary Artery Disease Congestive Heart Failure Valvular Heart Disease Athletic Heart Syndrome

3 Coronary Artery Disease (CAD) Arteries on the walls of the heart are vital to the heart muscle s survival, providing oxygen and necessary nutrients The disease process begins when atherosclerotic plaque begins to build up in the arteries

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5 Coronary Artery Disease Atherosclerosis Begins with trauma to the intima of the arterial wall Trauma related to list of risk factors Media (consists of smooth muscle is exposed to circulation Thought to be the origin of lesion.

6 Atherosclerosis Platelet agitation at lesion site induce smooth muscle and endothelial replication Fatty streaks low density lipoproteins (LDL) develop in smooth muscle of media Fibrous Plaque then develop impinging lumen Plaque consists of connective scar like tissue, smooth muscle, and fat.

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8 CAD Overtime, build-up of plaque can lead to arterial occlusion, which can cause a devastating blockage which will decrease or cut off oxygen to the myocardium Major risk factors for CAD: Smoking High blood pressure Diabetes > 45 years old (men) > 55 years old (women) Family history

9 Angina Pectoris Chest pain related to myocardial ischemia May be referred to left shoulder, neck, jaw, or between scapula. Anywhere above umbilicus could be anginal pain Three types

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11 Stable Angina Brought on by physical effort or stress Usually substernal nonradiating pain Last 5 to 15 minutes after stopping stressor Subsides completely with treatment Sublingual nitrate (nitro)

12 Unstable Angina Brought on by same triggers as stable angina Occurs more frequently Duration greater than 15 mins Intensity of pain more severe Indication of progression of CAD Increased risk for MI Less responsive to treatment can require hospitalization with IV nitrates.

13 Variant Angina Occurs at rest- during waking hours Not influenced by exertion Dysrhythmias occur Caused by stenosis and coronary artery spasm Treated with Ca Channel Blockers

14 Myocardial Infarction (MI) Necrosis of a portion of the myocardium Characterized by location, size and degree of involvement Location-anterior, posterior, lateral, inferior Size- large, small Transmural (full wall), subepicardial, subendocardial.

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16 Myocardial Infarction Uncomplicated- small infarction, inferior portion of heart partial wall thickness = full recovery Complicated MI- one or combination of dysrhythmia, heart failure, thrombosis, damage to heart structure. Prognosis is dependent on extent of damage to the ventricles

17 Congestive Heart Failure The inability of the heart to produce adequate cardiac output due to a structural or functional problem- impairing the ability of the heart to fill and pump blood adequately

18 Prevalence Estimated 23 million in the world Most common cause of hospital admission in the U.S. for patients older than million in the United States alone (Dupree) 600,000 cases diagnosed each year 1 million hospitalizations Records 1 out of 8 deaths $34.8 million a year (2008)

19 CHF More prominent in: Older population (>65) More men than women 4-6x more likely to die of heart disease than breast cancer Kills more women over 65 than all cancers combined Reported depression in 25-50%

20 Risk Factors Coronary artery disease It affects the heart by restricting or blocking the flow of blood Strongest risk factor in both men and women Smoking

21 Main Risk Factors Cont... Hypertension Preexisting hypertension is present in 75% of heart failure cases in the United States Previous MIs Diabetes More in women; associated with a 2-5 fold increase in heart failure Obesity Valvular disease

22 Other Risk Factors Anemia Thyroid Toxic agents: cocaine, alcohol, nonsteroidal agents Albuminuria Viruses/Infections Allergic reactions Blood clots in the lungs Dyslipidemia Chronic kidney disease Sleep-disordered breathing

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25 Valvular Heart Disease Congenital or Acquired Acquired- bacterial or viral infection of the heart valves Common over age of 65 Some do not require treatment Mitral Valve prolapse common in women vs men

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27 Athletic Heart Syndrome Cardiovascular adaptation to intense exercise can mimic disease process Sudden cardiac death in athletes usually caused by hypertrophy, dysrhythmia or both. Can be manifestation of congenital abnormalities in electrical or mechanical function of the heart.

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29 Cardiac Action Potential Phase 0- depolarization- Na+ channels open Phase 1-prolonged action potential due to slow and extended opening of Ca channels - repolarization begins. Phase 2-outward flow of K+ and prolonged opening of Ca lead to a plateau phase Phase 3- closure of Ca channels and opening of K channels completes repolarization. Phase 4- resting phase Na and Ca are pumper out K is pumped in.

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35 EKG 12 Lead (view) of the heart Six Leads record frontal plane Six Leads record transverse plane

36 Frontal Plane Leads 3 Bipolar limb leads I, II, III Single positive and single negative electrode 3 augmented unipolar limb leads avr (right arm) avl (left arm) avf (left leg) Have single positive lead derive negative from a combination of other electrodes.

37 Einthoven s Triangle

38 Bipolar Leads

39 Bipolar Limb Leads Lead Negative Electrode Positive Electrode Angle (degrees) Lead I RA LA 0 Lead II RA LL 60 Lead III LA LL 120

40 Augmented Leads

41 Augmented Leads Lead Formula Angle (degrees) avr RA (LA+LL) / avl LA (RA+LL) / 2-30 avf LL (RA+LA) / 2 90

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43 Axis Deviation

44 Axis Deviation

45 Precordial (transverse plane) Leads V 1-6 V1 and V2 look at R Ventricle V3 and V4 look at the intraventricular septum V5 and V6 look at L Ventricle

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47 EKG Evaluation What is the rate and pattern (regularity) is R-R interval equal for each beat? Is the a P wave before each QRS? = atrial Is the a QRS after every P wave?= conduction of atria to the ventricles P-R interval? Normal= seconds > 0.2 seconds= conduction delay or block QRS normal duration (0.1 sec) and shape?

48 Calculating Rate

49 Calculating Rate Count the number of small boxes between two R waves and divide into Count the number of R waves in a six second strip and multiply by 10.

50 Lets try it

51 Sinus Rhythms Sinus Rhythm bpm Sinus Bradycardia- < 60 bpm Sinus Tachycardia- > 100 bpm These rhythms have normal P waves, PR int and QRS int

52 Supraventricular Dysrhythmias Atrial and junctional Mechanisms SVT Atrial tachycardia Atrial Flutter Atrial Fibulation Junctional Rhythm

53 SVT Rate regular rhythm- no visible P waves- PR not measurable- QRS.12 or less

54 Atrial Tachycardia Rate regular- 1 P per QRS- PR may be shorter, QRS.12 or less

55 Atrial Flutter Atrial rate ventricular varies- Atrial is regular- ventricular can be irregular- P wavesaw tooth- PR not measurable- QRS <.12.

56 Atrial Fibrillation Rate can vary- Irregularly Irregular- P waves chaotic- PR not measured- QRS <.12.

57 Junctional Rhythm Rate regular- P waves inverted-before or after QRS or absent- PR if present <.12- QRS.12 or less.

58 Ventricular Dysrhythmias Premature Ventricular Contraction (PVC) Bigiminy Ventricular couplet Multifocal PVC (>1 etopic focus) Ventricular Tachycardia Ventricular Fibrillation

59 PVC Rate varies- Can be regular or irregular- P wave will be absent- unmeasurable PRI- QRS >.12.

60 Bigiminy 1 PVC every other beat- regular-irregular rhythm

61 PVC occurs twice Ventricular Couplet

62 Multi-Focal PVC Can be both positive and negative since there are different etopic origins

63 Ventricular Tachycardia 3 or more PVC with rate >100 bpm- patient can be asymptomatic- symptomatic or unconscious and pulseless.

64 Ventricular Fibrillation No organized rhythm- needs immediate defibrillation

65 Atrioventricular Blocks First Degree AV Block Second Degree AV Block Mobitz Type 1- Wenckebach Mobitz Type 2 Third Degree AV Block

66 First Degree Heart Block PR interval >.20

67 Mobitz Type 1 PR interval progressively get longer than QRS drops

68 Mobitz Type 2 Regular dropped QRS every 2 nd third or 4 th P wave- consistent PR interval

69 Third Degree Heart Block No conduction between A and V- both will have regular rates- Ps can be hidden in QRS

70 Story of the AV block Family

71 Bundle Branch Blocks Right Bundle Branch Block RBBB Left Bundle Branch Block LBBB

72 Left Bundle Branch Block Increased QRS >.10s Once a widened QRS > 0.10s is identified, we look at leads closest to the LV to identify a LBBB. Leads V5,V6, I, and avl are in close proximity to the left ventricle, and as such, are the best location to identify a LBBB. Characterized by an RSR segment or notched QRS

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74 Right Bundle Branch Block Look at Right chest Leads V1 and V2

75 Myocardial Infarction ST segment elevation ST segment depression Inverted T wave

76 ST segment elevation Transmural MI Use precordial leads to localize

77 ST segment depression Myocardial ischemia- can be diagnostic during exercise

78 Inverted T wave Myocardial ischemia (can be old)

79 Lets Give it a Try EKG Slides

80 Case 1

81 Case 2

82 Case 3

83 Case 4

84 Case 5

85 Answers EKG # Rate Regularity Axis Name of Rhythm Would you work with them? Why/Why not regular RAD 2 48 regular Normal Sinus Tachycardia Junctional Rhythm Yes if stable BP and no report of SOB or CP will monitor closely Depends on condition- would be very concerned about BP 3 60 Irregular Normal A-fib with bradycardia- ST depression No- there is ischemia would stop all activity 4 60 Regular LAD STEMI No way 5 75 Regular Normal 1 st degree heart block Yes- unless symptomatic